Absite 2009

Front 1

Breast

Front 4

Breast CA risk factors

Back 4

early menarche, late menopause, advanced age at first gestation, family history in first degree relatives, history of prior breast CA, lobular carcinoma in situ, atypical hyperplasia in fibrocystic disease, living in Western/Industrialized countries.

Front 5

Moderate Risk

Back 5

Atypical ductal or lobular hyperplasia

Front 7

Screening for Breast CA

Front 9

Palpable Breast Mass (self and physical exam) – Physical examination 55% sensitive at detecting existing breast CA. If palpable mass - Ultrasound or FNA first then A) if cystic, then aspirate and f/u U/S 6 weeks B) if solid FNA/Core to obtain cytology C) if solid w/ benign FNA/Core excise w/o margin D) Malignancy – appropriate locoregional tx

Front 11

Fibroadenoma -

Back 11

Most common breast tumor in women <35 years. Generally freely moveable under skin.

Front 13

Mammogram –

Back 13

Annual after age 50; q2 years after age 40. Start earlier with increased risk factors; 10% false negative and 10% false positive rates; reduce breast CA specific mortality but not overall mortality. Non-palpable detectable lesions BX via stereotactic (less expensive/morbid) or needle localization excisional bx (can be therapeutic).

Front 15

Infiltrating Ductal Carcinoma

Back 15

The most common form of breast cancer. Local excision w/ margin at least 2mm + sentinel lymph node mapping + XRT Vs. MRM (sentinel node w/ MRM acceptable)

Front 17

Inflammatory Breast Cancer

Back 17

histologically defined by tumor infiltration of the dermal lymphatics modified. Warmth, eythema, edema and tenderness. Peau d"orange. Tx

Front 19

Paget’s Disease of Nipple

Back 19

Variant of ductal carcinoma (in-situ or invasive) that extends to involve the epidermis of the nipple. Eczematous change in nipple skin. Underlying CA determines prognosis.

Front 21

Lobular CA in situ (LCIS) -

Back 21

Disease of breast lobules/acini, average age 45. No palpable mass or mamogram findings, always incidental finding on Bx. 1/3 develop CA in 20 years (equal risk in both breasts). Followup closely, tamoxifen, or bilateral mastectomy if strong family history.

Front 23

DCIS

Back 23

Histological cancer cells without basement membrane penetration. Comedo type (virulent), cribriform/papillary type (less likely to form palpable mass). Half develop into invasive cancer. Standard treatment = lumpectomy w/ 5mm margin and XRT. XRT proven to reduce recurrence and invasive CA. Mastectomy with 1cm margins w/ XRT for high grade, >2.5cm lesion, and multicentricity. Comedo type have necrotic cellular debris, microcalcifications, increased mitosis associated and has higher CA risk. No LN dissection unless > 2.5 cm or DCIS w/ Comedo type, microinvasion, or multicentricity.

Front 25

Intraductal Papilloma -

Back 25

Most common cause of spontaneous bloody nipple discharge. Treatment is total excision. No risk of cancer. (CA found in 5% of all bloody nipple discharges)

Front 27

Cystosarcoma Phylloides - The most common non-epithelial breast cancer. Tx

Back 27

Wide excision with free margins. If malignant or recurrent, mastectomy. Chemo for mets. No need for axillary sampling b/c hematogenous spread (like other sarcomas) when metastatic.

Front 29

Most common cause of unilateral ductal discharge

Back 29

intraductal papilloma. Fibrocystic changes of cystic mastopathy produces multiple not unilateral duct discharge.

Front 31

Angiosarcoma, High grade Tx

Back 31

Mastectomy and chemoradiation postop

Front 33

BRCA I -

Back 33

Chrom 17, tumor suppressor gene, 85% cancer by age 70, ovarian CA (45%), colon CA (in men prostate cancer). Accounts for 40% of familial breast cancer syndromes.

Front 34

BRCA II -

Back 34

Chrom 13, male breast cancer, ovarian CA (30%)

Front 35

Both tumor suppressor genes. If breast CA before age 45 with 1st degree relative, consider genetic testing. 5-10% of Breast CA associated with germline mutation.

Back 35

BRCA I AND II

Front 37

Tumor Marker

Back 37

CA 15-3 is elevated in 73% of patients with breast CA

Front 39

Tamoxifen

Back 39

selective estrogen receptor modifier, competitively inhibits estrogen effect on ER/PR+ patients; use for 5 years; increased risk DVT and endometrial CA b/c partial estrogen agonist; 50% annual recurrence reduction w/ tamoxifen use.

Front 41

Arimadex (Anastrozole)

Back 41

Inhibits estrogen synthesis (aromatase inhibitor). For ER+ patients proven slightly more effective than tamoxifen (ATAC trial) with significant decrease in DVT and endometrial CA.

Front 43

Herceptin

Back 43

monoclonal antibody to Her-2/neu (a growth factor receptor); applicable to PTs with Her-2/neu overexpression and positive lymph nodes/mets.

Front 45

Surgical Anatomy

Front 46

Winged scapula -

Back 46

injury to long thoracic nerve (serratus anterior)

Front 47

Difficulty with pull ups/adduction -

Back 47

injury to thoracodorsal nerve (latissmus dorsi)

Front 48

Loss sensation to medial arm -

Back 48

injury to intercostobrachial nerve

Front 50

Levels of axillary nodes

Front 51

Level I

Back 51

Lateral to the border of pectoralis minor

Front 52

Level II

Back 52

Under pectoralis minor

Front 53

Level III

Back 53

Medial to pectoralis minor (included in Halsted"s radical mastectomy but not in MRM)

Front 55

TN

Back 55

T1<2cm, T2 2-5cm, T3>5cm, T4 skin or chest wall involvement. N1 nodes, N2 fixed nodes, N3 ipsilateral int. mamm. nodes; M1

Front 58

T N M

Front 59

Stage I

Back 59

T1 N0 M0

Front 60

Stage IIA T0 N1M0

Front 61

T1 N1 M0

Front 62

T2 N0 M0

Front 63

Stage IIB T2 N1 M0

Front 64

T3 N0 M0

Front 65

Stage IIIA T0 N2 M0

Front 66

T1 N2 M0

Front 67

T2 N2 M0

Front 68

T3 N1 M0

Front 69

T3 N2 M0

Front 70

StageIIIB T4 Any N M0

Front 71

Any T N3 M0

Front 72

Stage IV Any T Any N M1

Front 74

CARDIAC

Front 77

CRITICAL CARE

Front 78

Intraaortic Balloon Pump

Back 78

Can be placed at bedside. Augments preload by inflating during diastole (40msec before T-wave). Reduces afterload by deflating during systole (deflates with P wave or start of Q wave). Increases diastolic blood flow, which increases coronarz perfusion. Common indications include acute myocardial infarction with shock and acute mitral insufficiency. Contraindication is aortic regurgitation.

Front 79

Tension Pneumothorax

Back 79

Decreases venous return by compressing IVC/SVC.

Front 80

Aortic Dissection

Back 80

Common cause of sudden death.

Front 81

Type A (I and II)

Back 81

Involves the ascending aorta. Can cause mediastinal rupture and cardiac tamponade, and requires immediate operation.

Front 82

Type B (III)

Back 82

Does not involve the ascending aorta and is medically managed by controlling HTN, however, surgery is required if signs of leg, renal, or visceral ischemia is present.

Front 83

Swan-Ganz Catheter

Back 83

Pulmonary vascular resistance (PVR) can only be measured with a Swan. Mal-position is the number one cause for loss of wave form. To be accurate, must be in Zone III of the lung.

Front 84

Beta-Blockers

Back 84

Cardio-protective pre-operatively. Can also be used to control ventricular response to atrial flutter.

Front 86

CARDIAC DISEASE

Front 88

CABG Indications

Back 88

Moderate to severe angina refractory to medical therapy, >50% left main, triple vessel disease, 70% LAD + one other vessel.

Front 89

Perioperative Mortality

Back 89

1% mortality risk from CABG. The #1 risk factor for periop mortality is emergency operation.

Front 90

Conduits

Back 90

IMA (first branch off subclavian) is the best conduit with patency rate of 95% at 20 years. Vein graft has 80% patency at 5 years.

Front 91

Angioplasty

Back 91

20% restenosis at 1 year.

Front 92

Acute Myocardial Infarction

Back 92

Complications include ventricular free wall rupture (VSD), mitral regurgitation (MR) from ruptured papillary muscle, and left ventricular aneurysm. Holosystolic murmur after MI suggests either VSD or MR.

Front 93

Post-op Pump Failure (CHF)

Back 93

Will have picture of cardiogenic shock, with increased PCWP, decreased CO, and increased SVR.

Front 94

Treatment

Back 94

Dobutamine drip.

Front 95

Myocardial Oxygen Demand

Back 95

Proportional to ventricular wall tension.

Front 97

CONGENITAL DEFECTS

Front 99

VSD

Back 99

Most common congenital cardiac defect. About 50% will close on their own. Surgery reserved for those with failure to thrive.

Front 100

Transposition of Great Arteries (TGA)

Back 100

Associated with cyanosis and desaturation. Will present with cyanosis in first week of life.

Front 101

Tetraology of Fallot

Back 101

Most common congenital cardiac defect that manifests as cyanosis.

Front 103

THORACIC

Front 106

CRITICAL CARE

Front 108

Tidal Volume (TV)

Back 108

Volume expired during normal breathing.

Front 109

Residual Volume (RV)

Back 109

Volume left in lung after maximal expiration.

Front 110

Expiratory Reserve Volume (ERV)

Back 110

Forced volume expired after end of normal TV breath

Front 111

Functional Residual Capacity (FRC)

Back 111

Volume left in lung after a normal breath. FRC=RV + ERV. FRC is decreased from atelectasis, ARDS, and pulmonary contusions.

Front 112

Residual Volume

Back 112

Volume left after maximal expiration (1-2.4L in adults)

Front 113

Total Lung Capacity (TLC)

Back 113

Volume after maximal inspiration.

Front 114

Vital Capacity

Back 114

Volume expelled after maximal inspiration and maximal expiration. VC= TLC-RV

Front 115

Pulmonary Function Test (PFT)

Back 115

Required before lung surgery.

Front 116

FEV1

Back 116

Forced expiratory volume in 1 second (after maximal inhalation). Must have predicted post-op FEV1 >0.8 to undergoe lung surgery.

Front 117

FEV1 Prerequisites

Back 117

Pneumonectomy 2L, Lobectomy 1L, and Wedge Resection 0.6L.

Front 118

Cricothyroidectomy

Back 118

When intubation fails. Needle cricothyroidectom for children <12 (45min. only, then intubate).

Front 119

Atelectasis

Back 119

Collapse of alveolar segments. Early ambulation decreases risk. Alveolar macrophages resopnsible for fever.

Front 120

Aspiration pneumonia

Back 120

Treat with nasotracheal suctioning and positive-pressure ventilation.

Front 122

LUNG CANCER

Front 124

Risk Factors

Back 124

Include tobacco and asbestos exposure.

Front 125

Presentation

Back 125

Cough, hemoptysis, chest pain, pleural effusion, and dypnea.

Front 126

Work-up

Back 126

CXR and CT of chest and abdomen (head if symptomatic).

Front 127

Diagnosis

Back 127

Percutaneous, or endoscopic biopsy. If biopsy twice fails to yield diagnosis, then thoracoscopic wedge resection.

Front 128

Histology is associated with location of lesion

Back 128

Centrally located lesions include Squamos Cell Carcinoma (SCC) 70%, Small Cell Carcinoma 80%, and Large Cell Carcinoma 60%. Peripherally located lesions inlude Adenocarcinoma 75% (which ist he most common lung CA)

Front 129

Carcinogenesis

Back 129

Commonly involves a point mutation involving the K-ras oncogene.

Front 130

Paraneoplastic syndromes

Back 130

Commonly associated depending on histologic type. SCC-Hypercalcemia from secretion of PTH. Small Cell Carcinoma- Cushing’s syndrome and SIADH from secretion of ACTH (most common) and ADH respectively.

Front 131

Resectability

Back 131

50-60% of patients will have direct metastasis at diagnosis.

Front 132

Staging

Front 133

Stage I

Back 133

N0, no direct invasion and >2 cm from carina

Front 134

Stage II

Back 134

N(+) ipsilateral hilar nodes, M0

Front 135

Stage III

Back 135

Invasion of adjacent structures (chest wall, diaphragm, pericardium) or mediastinal LN involvement.

Front 136

Stage IV

Back 136

M(+) distant metastases

Front 137

SVC Syndrome

Back 137

Swelling of the upper extremities and face. 90% of the time due to lung CA. Treatment is with Rx.

Front 138

Pancoast Tumors

Back 138

May involve the sympathetic chain, manifesting as Horner’s syndrome (ptosis, miosis, anhidrosis) and/or Ulnar nerve.

Front 139

Hamartoma

Back 139

Popcorn lesion seen on CXR. Most common benign adult lung tumor.

Front 141

OTHER CONDITIONS

Front 143

Chylothorax

Back 143

Thoracic duct empties into the left subclavian and internal jugular vein junction

Front 144

Treatment

Back 144

Initially 3-4 weeks of conservative treatment (medium chain triglycerides, TPN, chest tube). If that fails, surgery with ligation of the thoracic duct down low in the mediastinum.

Front 145

Thoracic Outlet Syndrome

Back 145

Usual presentation is neurologic symptoms in the C8-T1 distribution (Ulnar N.) in a middle aged woman. Symptoms are most commonly neural, not vascular. Therapy is based on anatomy involved.

Front 146

Nerve Involvement

Back 146

Initially treated non-surgically with physical therapy, if that fails then surgery.

Front 147

Subclavian Artery Involvment

Back 147

Initially treated with surgery.

Front 148

Subclavian Vein Involvement

Back 148

Initially treated with thrombolytics, heparin, and warfarin, if this fails then surgery

Front 149

Colorectal

Front 153

Appendicitis

Front 154

Etiology

Back 154

appendicolith (adults) or lymphoid hyperplasia (children) most common mechanism, also due to tumors (carcinoid=90%, adenocarcinoma)

Front 155

Diagnosis

Back 155

Physical exam and imaging. On CT will appear as periappendiceal inflammation (stranding), incomplete filling with contrast, appendix diameter >6mm, wall thickening and enhancement with IV contrast.

Front 156

Treatment

Back 156

Appendectomy unless perforated with walled-off abscess

Front 157

(IR drain, interval appendectomy)|

Front 159

Appendiceal Carcinoid

Front 160

Treatment

Back 160

If it is < 2 cm and/or at the tip, appendectomy is sufficient; if >2cm and/or at the base, need right hemicolectomy.

Front 161

How do you treat a cystic mass at base of appendix? Right hemicolectomy. Assume cystadenocarcinoma. Do not spill content.

Front 163

Colon Polyps

Front 164

Histology

Front 165

Hyperplastic polyps

Back 165

(most common) No malignant potential, hard to differentiate from neoplastic polyps, thus send for path.

Front 166

Inflammatory polyps

Back 166

In IBD, no malignant potential

Front 167

Juvenile polyps

Back 167

Hamartomas, can bleed, no malignant potential

Front 168

Adenomatous polyps

Back 168

Have malignant potential. Different malignant potential based on morphology (Villous > Tubulovillous > Tubular), and size (increasing size à increasing malignant potential).

Front 171

Colon Adenocarcinoma

Front 172

Carcinogenesis

Back 172

APC (tumor suppressor mutated in FAP), p53 (tumor suppressor) absent in 85%, K-ras (oncogene) in half patients, DCC deleted in 70%

Front 173

Staging

Front 174

T0

Back 174

in-situ

Front 175

T1

Back 175

invades submucosa

Front 176

T2

Back 176

invades muscularis propria

Front 177

T3

Back 177

invades through muscularis propria into serosa (but not through serosa)

Front 178

T4

Back 178

through serosa; direct invasion of adjacent structure or perforated cancer

Front 180

N0

Back 180

No nodes

Front 181

N1

Back 181

1-3 regional nodes

Front 182

N2

Back 182

4 or greater regional nodes

Front 184

M0

Back 184

No metastases

Front 185

M1

Back 185

Any distant metastases

Front 187

Dukes A/Stage I

Back 187

T1-T2, N0, M0 (90% survival)

Front 188

Dukes B/Stage II

Back 188

T3-T4, N0, M0 (75% survival)

Front 189

Dukes C/Stage III

Back 189

Any T, N1-2, M0 (45% survival)

Front 190

Dukes D/Stage IV

Back 190

Any T, Any N, M1 (10% survival)

Front 191

Treatment

Back 191

Based on stage. Need to resect with at least 3 cm margin bowel, with ligation of lympho-vascular supply to that segment.

Front 192

Stage I

Back 192

Segmental resection

Front 193

Stage II

Back 193

Segmental resection +/- adjuvant therapy

Front 194

Stage III

Back 194

Segmental resection with adjuvant chemotherapy

Front 195

(5FU+leucovorin, semustine, vincristine)

Front 196

Low tumors

Front 197

LAR (low anterior resection) when tumor is 5-10 cm from anal verge

Front 198

APR when < 5 cm from anal verge (controversial, now some say < 2cm)

Front 199

When can colorectal cancer be treated with just polypectomy

Front 200

during colonoscopy? > 2 mm margin, well-differentiated, no lymphovascular invasion (must meet all of these criteria)

Front 202

Anastomotic Leaks

Front 203

Management

Back 203

If mild (low grade fever, mild discomfort, malaise) may observe with Abx

Front 204

If abscess > 5cm - IR drainage

Front 205

If multilocular abscess, >50% of anastomosis circumference, or deteriorating clinical signs, then to OR for Hartman"s procedure

Front 207

Hepatic metastases

Front 208

Prognosis

Back 208

25% 5-year survival

Front 209

Diagnsois

Back 209

intra-op ultrasound can detect metastases down to 3mm.

Front 210

Treatment

Back 210

Cryotherapy—can’t use near major vessels, Trans-arterial chemoembolization, RFI, Ethanol ablation, surgical resection.

Front 212

Pulmonary metastases

Front 213

Prognosis

Back 213

20% 5-year survival if isolated and resectable

Front 214

Treatment

Back 214

can resect isolated mets.

Front 216

Lynch Syndrome (Hereditary Nonpolyposis Colorectal Cancer (HNPCC))

Front 217

Etiology

Back 217

Genetic defect in DNA mismatch repair gene. Most common hereditary colorectal CA in the west. Autosomal dominant inheritance.

Front 218

Presentation

Back 218

No polyposis (but can have polyps). Onset

Front 219

Detection

Back 219

colonoscopy at 20 years or at least 5 years earlier than

Front 220

earliest age of detection in family

Front 221

Types

Front 222

Lynch 1

Back 222

Right sided colon CA at early age (44)

Front 223

Lynch 2

Back 223

Colon CA and CA of ovary, bladder, gastric, small bowel

Front 224

#NAME?

Back 224

Autosomal dominant

Front 225

Treatment

Back 225

Subtotal colectomy (Lynch I), consider prophylactic hysterectomy, oophorectomy etc. in Lynch II (along with subtotal colectomy), screening critical (e.g. CA-125)

Front 228

FAP

Front 229

Etiology

Back 229

Germline loss of APC gene on chromosome 5. Autosomal dominant inheritance.

Front 230

Presentation

Back 230

Polyposis (>100 colonic adenomatous polyps) at an early age, usually shortly after puberty, more left-sided tumors than HNPCC, 100% penetrance by age 35, can develop hundreds to thousands of polyps. 100% lifetime risk of colorectal CA (~85% by age of 35).

Front 231

Treatment

Back 231

Definitive treatment is removing entire colon and rectum (total proctocolectomy with end ileostomy), however with low rectal polyp burden may perform IPAA with J-pouch with frequent rectal surveillance with proctosocopy. Also, sulindac (and now Celebrex) are used to decrease growth of polyps.

Front 233

Other polyposis syndromes

Front 234

Gardners Syndrome

Back 234

Colon cancer and desmoid tumor

Front 235

Turcot syndrome

Back 235

Colon cancer and brain tumors

Front 236

Peutz-Jeghers Syndrome

Back 236

hamartomas throughout GI tract,

Front 237

mucocutaneous tumors, hyperpigmentation, can cause obstruction, low risk of malignancy

Front 238

Cowden disease

Back 238

hamartomatous polyps with facial epithelial lesions, breast cancer

Front 239

Cronkhite-Canada syndrome

Back 239

Hamartomatous polyps, diarrhea, alopecia, hyperpigmentation

Front 241

Rectal Adenocarcinoma

Front 242

Staging

Back 242

Similar staging to colonic adenocarcinoma. Pre-op evaluation should include endorectal ultrasound to determine depth of invasion and lymph node disease

Front 243

Treatment

Back 243

Based on stage

Front 244

Stage I

Back 244

Segmental resection

Front 245

Stage II

Back 245

Segmental resection with adjuvant therapy

Front 246

Stage III

Back 246

Segmental resection with adjuvant chemotherapy

Front 247

Adjuvant therapy includes both radiation and chemotherapy

Front 248

UT3 cancers (ultrasound) need preop chemo and radiation

Front 249

Any node positive tumor needs preop chemo and radiation plus postop chemo

Front 251

Anal Canal Tumors (above dentate line)

Front 252

Squamous Cell Carcinoma

Back 252

most important prognostic factor is size

Front 253

Risk factors

Back 253

STDs, HPV, anal intercourse

Front 254

Treatment

Back 254

chemo and radiation (Nigro protocol); post-op cisplatin for residual disease,

Front 255

APR for persistent tumor after post-op chemo

Front 256

Melanoma

Front 257

Treatment

Back 257

WLE (same survival as APR, < 20%)

Front 258

AdenoCA of anal canal

Back 258

is extremely rare with poor prognosis

Front 260

Anal Margin Tumors (below dentate line)

Front 261

Bowen’s Disease

Back 261

squamous cell carcinoma in situ. Treatment is WLE.

Front 262

Paget’s Disease

Back 262

intraepithelial adenocarcinoma

Front 263

Basal Cell Carcinoma

Back 263

Treat with WLE.

Front 264

Squamous cell carcinoma of anal margin

Back 264

WLE

Front 265

Verrucous carcinoma

Back 265

WLE

Front 266

Kaposi’s sarcoma

Back 266

WLE + chemo/rads

Front 268

Colonic pseudo-obstruction (Ogilvie’s Syndrome)

Front 269

Etiology

Back 269

Neurological, electrolyte abnormalities.

Front 270

Presentation

Back 270

initially painless bowel distention with obstructive symptoms without radiographic signs of mechanical obstruction.

Front 271

Diagnosis

Back 271

Water-soluble contrast enema study, or colonoscopy

Front 272

Treatment

Back 272

In this order

Front 273

1. NGT and correction of electrolyte abnormality

Front 274

2. IV Neostigmine - stimulate parasympathetic pathway

Front 275

3. Colonic decompression with colonoscopy-success rate of endoscopic decompression = 80-90%; recurrence rate = 40%

Front 276

4. If don"t respond to above, then OR for ex-lap (cecostomy or if bowel necrotic, resection)

Front 277

-Cecum at greatest risk of perforation (Laplace’s Law

Back 277

Tension = Pressure x radius)

Front 279

Sigmoid Volvulus

Front 280

Epidemiology

Back 280

Acquired disease, caused by redundant sigmoid colon,

Front 281

accounts for up to 90% of colonic volvulus

Front 282

Risk factors

Back 282

elderly, nursing home patients, neurologic disorders

Front 283

Diagnosis

Back 283

plain film = dilated loop with point extending towards

Front 284

RUQ (bent inner tube), barium enema = bird’s beak; sigmoidoscopy

Front 285

Presentation

Back 285

early = distention, obstipation; later = peritonitis,

Front 286

elevated WBC, fever

Front 287

Treatment

Back 287

Early

Front 289

Cecal Volvulus

Front 290

Epidemiology

Back 290

Right colon isn’t completely fixed, accounts for 10%

Front 291

of colonic volvulus

Front 292

Diagnosis

Back 292

dilated loop with point extending towards LUQ

Front 293

Treatment

Back 293

Resection of right colon

Front 295

Diverticular Disease

Front 296

Etiology

Back 296

Diverticula are pseudodiverticula or false diverticular—outpouching

Front 297

doesn’t involve all layers of the colonic wall. Caused by increased intraluminal pressure (chronic constipation)

Front 298

Epidemiology

Back 298

Most common site is the sigmoid colon. Incidence

Front 299

Presentation

Back 299

LGIB (most common cause in adults) and diverticultis (can also be found on screening colonoscopy).

Front 300

Diverticulitis

Back 300

Occurs in 20% of those with diverticular disease.

Front 301

-20% develop complications after first attack, 60% after second

Front 302

#NAME?

Back 302

LLQ pain, fever, elevated WBC

Front 303

Treatment of diverticulitis

Front 304

a) localized inflammation, no abscess

Back 304

IV ABx, NPO, colonoscopy

Front 305

after inflammation ends; Before age 50 at time of first attack à elective

Front 306

1-stage resection after cools down; After age 50 at time of first attack à

Front 307

high fiber diet, resect after recurrence

Front 308

b) localized abscess

Back 308

IR drain, IV ABx à if improves, same as (a),

Front 309

if worsens, see below

Front 310

c) peritonitis, free perforation

Back 310

Hartman’s procedure

Front 312

LGIB (bleeding distal to ligament of Treitz)

Front 313

Etiology

Back 313

Diverticular bleeding (15% of patients with diverticula

Front 314

have at least one episode), Arteriovenous malformation (AVM), hemorrhoids, colorectal cancer, inflammatory bowel disease, ischemic colitis

Front 315

Most common causes in children

Back 315

#1 Meckel’s diverticulitis

Front 316

Most common causes in adults

Back 316

#1 Diverticular bleed

Front 317

Steps in Diagnosis/Treatment

Front 318

-Nasogastric lavage (rule out UGIB—EGD if positive)

Front 319

#NAME?

Front 320

#NAME?

Back 320

tagged red blood cell nuclear

Front 321

scan to localize - IR for embolization if possible, ex-lap if treatment fails

Front 322

#NAME?

Front 323

-Total abdominal colectomy if non-localized and (> 6u transfused in 24h)

Front 324

uncontrolled (can try intra-operative colonoscopy to localize in operating room)

Front 326

Pseudomembranous Colitis

Front 327

Etiology

Back 327

antibiotic-associated colitis caused by C. difficile

Front 328

Symptoms

Back 328

watery diarrhea, crampy abdominal pain

Front 329

Diagnosis

Back 329

ELISA for toxin A or B; sigmoidoscopy (pseudomembranes)

Front 330

Treatment

Back 330

po flagyl > IV flagyl; alternative = po vancomycin (no effect IV); cholestyramine binds toxin; no antimotility (loperamide) agents

Front 332

Hemorrhoids

Front 333

Internal

Back 333

painless rectal bleeding, prolapse

Front 334

External

Back 334

painful, burning, itching

Front 335

Treatment

Back 335

Internal (Sitz baths, stool softeners, hemorrhoidectomy if irreducible or perpetually prolapsed). External (Sitz baths, stool softeners, I & D if present within the first 48 hours)

Front 337

Rectal prolapse

Front 338

Incidence

Back 338

more common in women (increased risk with childbearing)

Front 339

Presentation

Back 339

anorectal discomfort, constipation, visible prolapse, incontinence

Front 340

Treatment

Back 340

Ripstein operation

Front 342

Anal Fissure

Front 343

Definition

Back 343

Linear tear in anal mucosa. Almost always in posterior midline; if lateral or multiple fissures = check for IBD/HIV

Front 344

Symptoms

Back 344

pain on defecation, bleeding

Front 345

Treatment

Back 345

High residue diet, sitz baths, stool softeners, NTG, Botox, lateral internal sphincterotomy if severe or no relief after 3 weeks of conservative management

Front 347

Fistula in Ano and Perianal Abscess

Front 348

-fistula in about 50% of cases of abscess

Front 349

Goodsall’s rule

Back 349

anterior fistulas connect with rectum in a straight line;

Front 350

posterior fistulas curve towards a midline internal opening in the rectum

Front 351

Treatment

Back 351

Fistulotomy or seton placement

Front 353

Inflammatory Bowel Disease

Front 355

UC Crohn’s

Front 356

Involves entire colon 20% No

Front 357

Involves distal colon Always Rare

Front 358

Involves small bowel rare Usually

Front 359

Skip lesions No Yes

Front 360

Pseudopolyps Yes No

Front 361

Transmural inflammation No Yes

Front 362

Granulomas No Yes

Front 363

Crypt abscesses Yes No

Front 364

Extraintestinal symptoms Parallels disease Yes

Front 366

Ulcerative Colitis (UC)

Front 367

Symptoms

Back 367

15% present acutely with bloody diarrhea, abdominal pain, fever. 85% present with chronic weight loss, abdominal pain

Front 368

Cancer risk with UC

Back 368

low risk first 10 years (2-3%). After 10 years, risk increases 1-2% per year [After 20 years, 10-20% risk]

Front 369

Medical Treatment of UC

Back 369

Sulfasalazine, steroids, azathioprine, 6-MP

Front 370

Indications for surgery for UC

Front 371

#NAME?

Front 372

#NAME?

Front 373

#NAME?

Front 374

#NAME?

Front 375

#NAME?

Front 376

#NAME?

Front 377

Procedures for UC

Back 377

Curative

Front 378

1) Total proctocolectomy with IPAA

Back 378

removal of entire colon, rectal mucosectomy/low rectal resection, ileal pouch (J, S, or W pouch)

Front 379

2) Total proctocolectomy with continent ileostomy

Front 380

3) Total proctocolectomy with end ileostomy

Front 382

Crohn’s Disease

Front 383

Symptoms

Back 383

abdominal pain, diarrhea. 55% affect both large and small bowel, 15% affect only large bowel

Front 384

Pathology

Back 384

Apthous ulcers and transmural inflammation

Front 385

Extrainestinal manifestation

Back 385

Uveitis, arthritis, erythema nodosum, pyoderma gangrenosum, iritis, spondylitis, sclerosing cholangitis, apthous stomatitis.

Front 386

Indications for surgery for Crohn’s

Back 386

Same as for UC including failure to thrive in children, except surgery is not curative.

Front 387

Duodenal crohn"s refractory to to medical therapy can be treated with gastrojejunostomy and vagotomy.

Front 389

Radiation Proctitis - occurs 8-12 months post radiation. May treat with formalin.

Front 390

Inhabitants of the colon

Front 391

> 95% anaerobes (Bacteroides fragilis)

Front 392

< 5% aerobes (E. coli, Enterococcus)

Front 395

Endocrine

Front 399

MEN1(Wermer Syndrome)

Back 399

Mnemonic- "Peter Pan had a Parathyroid" Peter= Pituitary, Pan= Pancreas, and Para=Parathyroid

Front 401

Parathyroid

Back 401

~95% develop it, early onset ~25y.o, Hyperplasia rather than adenoma as in sporadic cases, must rule out familial hypercalcemic hypocalciuria and hypercalcemia exacerbates ZE syndrome Dx

Front 402

Pancreas/Duodenum

Back 402

~35-75% of pts with MEN I

Front 403

#NAME?

Back 403

most common functional tumor, thought to be in gastrinoma triangle but more located within the duodenum or within peripancreatic lymph nodes, aggressive and high malignant potential Dx

Front 405

#NAME?

Back 405

second most common tumor, Whipple"s triad

Front 407

3)Pituitary

Back 407

~16-65% a/w anterior pituitary adenomas, most commonly prolactinoma, Cushing"s dx is rare

Front 409

Genetics

Back 409

On chromosome 11q13, tumor suppressor gene which produces a protein product called MENIN, a nuclear protein

Front 411

Treatments

Front 413

Hyperparathyroidism

Back 413

-total parathyroidectomy with autotransplantation or 3 1/2 parathyroidectomy

Front 414

Pancreas

Back 414

Medica treatment with PPIs, parathyroidectomy improves the symptoms of ZE syndrome, controversial when to excise but size related to malignant potential, long-term use of omeprazole a/w gastric carcinomas

Front 415

Pituitary

Back 415

for Prolactinoma use bromocriptine, transphenoidal resection for enlarging adenoma or refractory medical treatment

Front 416

MEN2A(Sipple Synrome)

Front 418

1)Medullary Thyroid Carcinoma

Back 418

virtually 100% develop it by 2nd or 3rd decade, presence of amyloid in the stroma is diagnostic, parafollicular C cells, can be a/w Familial non-MEN medullary thyroid cancers that usually present in the 5 to 6th decades Dx

Front 420

2) Pheochromocytoma

Back 420

~50% develop it, it may be bilateral, ectopic location at organ of Zuckerkandl(at aortic bifurcation) Dx

Front 422

3)Parathyroid

Back 422

~30% develop it

Front 424

***** MEN IIA can be a/w Hirshprung"s Disease in infants

Front 427

MEN2B

Front 429

1)Medullary Thyroid Cancer

Back 429

-Earlier presentration, 1st decade

Front 431

2)Pheochromocytoma

Front 433

3)Neuromas, Marfanoid Habitus

Front 435

Genetics of MEN II

Back 435

-Ret-Proto Oncogene, on chromosome 10, encodes a transmembrane receptor tyrosine kinase that functions in signal transduction.

Front 437

Treatment

Front 439

MTC

Back 439

Early detection and surgical resection is key, Total thyroidectomy with central node dissection as early as possible, MTC is not chemo or XRT sensitive

Front 441

Pheochromocytoma

Back 441

must rule out Pheo prior to thyroid surgery, some advocate Bilateral Adrenalectomy because frequently bilateral, and not a/w Addison"s disease after surgery and some advocate Unilateral Adrenalectomy because ~50% did not develop is on the other side after 10 years, if Malignant, bilateral resection is indicated

Front 443

Parathyroid

Back 443

As mentioned above for MEN I

Front 447

Thyroid Cancer

Front 449

1) Papillary carcinoma

Back 449

makes up two-thirds of all thyroid cancers, most common histologic type a/w prior neck irradiation. Female prediminance is 3

Front 451

Dx

Back 451

FNA or Core biopsy

Front 453

Management

Back 453

mainstay of management is surgery. Extent of surgery is controversial. 2 school of thoughts.

Front 455

a) Thyroid lobectomy and isthmectomy-preserves thyroid function and in most cases will adequately resect the lesion. The downside of this approach is that post-operative I-131 scanning is not possible since the isotope will be taken up by the remaining thyroid gland and therefore will not be useful for detecting metastases or recurrences.

Front 457

b) Total Thyroidectomy- allows for post-operative I 131 scanning and ablation if residual or metastatic disease is detected. Also ensures that all possible foci of tumor are removed. Can use serum thyroglobulin levels post-operatively as an early sign of recurrence. The downside is that patients will require lifelong thyroid hormone replacement.

Front 459

While the choice of operation is surgeon dependent, there are some situations where a total thyroidectomy is probably the procedure of choice. These are

Back 459

AGES- Age>50 years(women) or >40 years(men), Grade is poorly differentiated, insular, mucoid or tall cell, Extent of invasion is into adjacent tissues and Size of lesion is greater than 4 cm.

Front 461

Lymph node dissection is advocated only in the presence of grossly involved nodes. If nodes are positive at the time of thyroid resection, an ipsilateral modified radical nect dissection can be performed.

Front 463

Prognosis

Back 463

Can be cured in >90 %.

Front 465

Follow-Up

Back 465

routine physical exam, I-131 scanning and serum thyroglobulin levels if a total thyroidectomy was performed and imaging such as CT and MRI in cases where an aggressive variant was present. Local recurrences can be managed with surgical resection or external beam radiotherapy as well as I-131 ablation. Distant disease can be managed with I-131 ablation, surgical resection or chemotherapy. For patients undergoing I-131 scanning, T4(thyroxine) needs to be withdrawn as TSH needs to be elevated in order to stimulate iodine uptake. For this reason, patients are often given T3(cytomel) prior to planned scanning since it has a much shorter half life.

Front 467

2) Follicular carcinoma

Back 467

comprises 25% of thyroid cancers, peak incidence later than papillary(5th decade). Female predilection is also seen. Metastatic spread is hematogenous rather than lymphatic spread. The most common sites of distant spread are to bone, lung and liver. Metastatic foci can concentrate iodine and therefore can be treated with I-131 ablation.

Front 469

Dx

Back 469

distinction between follicular adenoma and follicular carcinoma cannot be made on FNA or frozen section. If a lesion is diagnosed as follicular neoplasm on FNA, lobectomy must be done to make the diagnosis.

Front 471

Management

Back 471

Surgery is mainstay of treatment. Total thyroidectomy is more often recommended owing to the utility of post-operative I-131 scanning for the detection and then possible ablation of distant metastases. Post-operative suppression of TSH has been shown to be of benefit.

Front 473

Lymph node involvement is less common than in papillary cancer, however, if nodes are involved they are removed in a similar fashion.

Front 475

Prognosis

Back 475

10 year survival rate is slightly worse than papillary but it ranges from 45 to 95% in the literature.

Front 477

Follow-up

Back 477

same as papillary with addition of scans to assess for metastatic disease.

Front 479

Hurthle cell tumors are thought to be a follicular variant that can behave in a more aggressive fashion. They can spread via lymphatics like papillary lesions. They are managed in a similar fashion to follicular cancers.

Front 481

3)Medullary carcinoma

Back 481

less common, they produce calcitonin, which can be used for both screening and detection of recurrence. The presence of amyloid in the stroma of these tumors is diagnostic. It can be part of MEN II, FMTC(familial non-MEN medullary thyroid cancer), or sporadic cases. The familial forms are multicentric in 90% of cases while 20% in sporadic forms.

Front 483

Dx

Back 483

elevated serum calcitonin level and on biopsy

Front 485

Management

Back 485

surgical, total thyroidectomy with central lymph node dissection is the standard operation. A lateral neck dissection is performed if these nodes appear to be involved.

Front 487

Prognosis

Back 487

patients with MEN IIA and FMTC have a better long term outcomes than those with MEN IIB or sporadic tumors. 10 year survival ranges from 30-60%.

Front 489

Follow-up

Back 489

serum calcitonin and physical examination. Recurrences are managed with repeat resections.

Front 491

4)Anaplastic carcinoma

Back 491

it accounts for 10% of thyroid cancers and is the most aggressive form. It is typically seen in the sixth decade and can be very aggressive locally as well as metastasize widely. External beam radiation therapy can be used to control local disease and main role for surgery is in the performance of a tracheostomy to prevent airway obstruction. Chemotherapy can be used but is not often successful.

Front 493

5)Lymphoma

Back 493

involving the thyroid can be seen and is treated as are other lymphomas with a combination of chemotherapy and radiation. In some cases, surgery is used to manage large thyroids causing compressive symptoms.

Front 495

Grave"s Disease

Back 495

is a systemic autoimmune disease that includes goiter, thyrotoxicosis and ophthalmic signs such as upper lid spasm, external opthalmoplegia, exophthalmos with proptosis, supraorbital and infraorbital edema and conjunctival congestion. Treatment includes medical management consisting of antithyroid drugs or radioactive iodine versus surgical resection. Commonly used medications include methimazole, and propylthiouracil. In response to medications, a normal metabolic rate can be regained in approximately 6 weeks. However, recurreces after drug withdrawal occur in 75% of patients. While radiation therapy has a high success rate(remissions in 80-98% of patients) it can lead to permanent hypothyroidism, development of thyroid nodules and is contraindicated in pregnant or lactating women. Surgery generally consists of a subtotal thyroidectomy with a rim of thyroid tissue left along the parathyroids. Surgery is successful in over 95% of patients but is is not without risks which include recurrent laryngeal nerve injury, hypoparathyroidism (1-3%), hypothyroidism (10-30%) and recurrence of hyperthyroidism(2-12%). Pre-operative treatment to avoid thyroid storm and to decrease the size and vascularity of the gland is often performed. Antithyroid drugs are administered, iodine is given 8-10 days prior to surgery(to decrease vascularity) and beta-blockers such as propranolol are used. While thyroid strom is not commonly seen, it still can occur following surgery for thyrotoxicosis. It is manifested by hyperthermia, tachycardia, hypertension, and eventual hypotension and death. It is due to a massive adrenergic outburst augmented by the presence of thyroid hormone. Treatment consists of large doses of propranolol, IV iodine, steroids, glucose, and oxygen. Mortality is ~10%.

Front 497

Nontoxic multinodular goiter

Back 497

may be due to endemic conditions of iodine deficiency, impairment of iodine uptake by the thyroid caused by congenital defects or due to TSH hypersecretion. Patients may by hypothyroid. Thyroid hormone replacement to suppress TSH release is used. Surgery may be used to manage large glands causing compressive symptoms and is generally a subtotal thyroidectomy.

Front 499

Toxic multinodular goiter- can be seen in patients with a history of nontoxic multinodular goiter and is secondary to a nodule becoming autonomously functional. This is known as Plummer"s disease and is usually not as severe as Grave"s disease. Surgery is the treatment of choice since medications and radioactive iodine are not effective.

Front 501

Thyroiditis

Back 501

is not commonly managed by surgeons but can lead to thyroid nodules and therefore the surgeon should be familiar with the common types that are seen.

Front 503

Hashimoto"s thyroiditis

Front 504

acure suppurative thyroiditis

Front 505

subacute thyroiditis

Front 506

Riedel"s struma

Front 507

Parathyroid Disease

Front 509

1)Primary Hyperparathyroidism- it accounts over 90% with malignancy as the cause of hypercalcemia and most common cause in outpatients. Most often due to a single hyperfunctioning hypercellular parathyroid gland, which is hypersecreting PTH but may be due to sporadic multigland disease in as many as 5-10%.

Front 511

Sx

Back 511

nephrolithiasis, bone pain, bone density loss, abdominal cramps and depression or psychoses.

Front 513

Dx

Back 513

hypercalcemia a/w elevated PTH and presence of increased urine calcium on a 24 hour urine collection.

Front 515

Tx

Back 515

95 % are cured with excision of adenoma, if it recurs then localizing studies must be done to look for missing glands. Ultrasound, sestamibi scan, CT and MRI for imaging studies. Invasive studies have relied on venous sampling and arteriography. Ectopic glands can be found high or undescended in the pharynx or along the carotid sheath or low in the thymus or mediastinum. At the time of a first neck exploration, it is not recommended to perform a sternotomy in an attempt to locate a missing inferior gland. Closing the neck and proceeding to localization studies is more prudent. The role of a blind thyroid lobectomy is controversial as intrathyroidal glands are uncommon.

Front 517

2)Secondary hyperparathyroidism

Back 517

results from a compensatory response of normal parathyroids to a lowered serum calcium brought on by renal disease or malabsorption. In the case of renal disease this is due to a lack of production of 1,25-dihydroxyvitamin D and decreased phosphate excretion. Clinical manifestations include bone pain, pathologic fractures, nausea, vomiting, ulcer disease and painful extraskeletal calcifications. Surgical management consists of either a 3 1/2 gland parathyroidectomy or total parathyroidectomy with autotransplant.

Front 519

3)Tertiary hyperparathyroidism

Back 519

occurs in the course of secondary hyperparathyroidism when the associated chief cell hyperplasia appears to become autonomous. The most common situation is persistent hyperparathyroidism following a successful renal transplant. The preferred management is conservative.

Front 522

Adrenal

Front 524

1) Incidental mass

Back 524

noted on up to 2% of CT scans of the abdomen. The most common lesion detected as an incidental mass is a non-functioning cortical adenoma. These lesions are small, homogeneous and may be bilateral and multiple. They tend not to enhance with IV contrast. Since most adrenalcortical carcinomas tend to be greater than 6 cm in size, small non-functional lesions can be observed without the need for any surgical intervention. The workup of an incidental adrenal mass involves a careful measurement of size, a careful history including history of hypertension, weight gain, bruisability, diabetes etc. Based on suspicions raised by history or physical exam, appropriate laboratory tests can be ordered. If the work up of a lesion less than 6 cm is negative, observation is appropriate.

Front 526

2) Functional cortical adenomas

Back 526

include glucocorticoid producing adenomas and aldosterone producing adenomas. The appropriate treatment is resection. Patients with steroid producing adenomas may present with signs and symptoms of Cushing"s syndrome and the appropriate workup for a non-pituitary source should be performed including serum and urine cortisol, low and high dose dexamethasone suppression tests. Aldosterone producing adenomas lead to hypertension and hypokalemia. The workup includes 24 hour urine for aldosterone levels as well as measurement sof serum aldosterone and renin activity. Selective venous sampling can be used to lateralize these often small lesions. Need to distinguish if it is due to adenoma(80%) vs hyperplasia, because if hyperplasia the treatment is aldactone not surgery.

Front 528

3) Pheochromocytoma

Back 528

most common active tumor found in the adrenal. They are a/w hypertension, palpitations, anxiety and diaphoresis. They can be associated with MEN syndromes, VHL and von Recklinghausen disease. The lesions are generally contrast enhancing on CT scan and the workup includes 24 hour urine collections for VMA, metanephrine and catecholamine levels. Ectopic locations in the midline near the aortic bifurfication can be seen(organ of zukerkandl). An MIBG scan can be helpful in localization. Management is by surgical resection after appropriate catecholamine blockade usually with phenoxybenzamine. Never beta block first without blocking the alpha receptors.

Front 530

4) Adrenocortical carcinoma

Back 530

usually unilateral and are generally 6 cm or larger in size when they are detected. They are aggressive tumors both locally and may spread to distant sites such as lymph nodes, lung, bone, liver and kidney. It can be fuctional leading to Cushings or virilization. The treatment is surgical resection and at present open resection of a suspected carcinoma is recommended.

Back 535

Esophagus

Front 539

Esophageal Cancer

Back 540

Epidemiology: Squamos Cell Carcinoma is most common histology worldwide (~95%). Adenocarcinoma is most common histology in U.S. (~60%).

Back 541

Presentation: Dysphagia, weight loss, difficulty swallowing solids. 70% will be non-resectable upon diagnosis.

Back 542

Prognosis: Average survival without esophagectomy is 6 months.

Back 543

Risk Factors: ETOH, tobacco, achalasia, nitrosamines (SCC). Tobacco, Barret’s esophagus (Adenocarcinoma). Barrett’s metaplasia raises risk 40x for adenocarcinoma.

Back 544

Indications for Surgery: High-grade Barret’s, and/or localized cancer.

Front 546

Leiomyoma

Back 547

Epidemiology: Most common benign tumor of the esophagus

Back 548

Presentation: Usually asymptomatic, but may cause dysphagia or retrosternal pressure/pain.

Back 549

Treatment: If symptomatic, or >5cm in size, submucosal enucleation.

Front 551

Zenker"s Diverticulum

Back 552

Etiology: Caused by increased pressure during swallowing. Occurs between thyropharyngeous and cricopharyngeous muscles.

Back 553

Presentation: May cause malnutrition or recurrent aspiration.

Back 554

Treatment: Cricopharyngeal myotomy with diverticulectomy.

Front 556

Epiphrenic Diverticulum

Back 557

Etiology: Esophageal dysmotility.

Back 558

Presentation: Can have dysphagia, regurgitation.

Back 559

Treatment: Diverticulectomy with long myotomy on opposite side of diverticulectomy.

Back 560

Etiology: Decreased lower esophageal sphincter tone.

Back 561

Treatment: Medical treatment first. If this fails, then fundoplication (over 80% success with this operation). Common cause of dysphagia after procedure is too tight of a wrap.

Front 563

Esophageal Perforation

Back 564

Presentation: Chest pain after forceful vomiting or iatrogenic after instrumentation.

Back 565

Etiology: Iatrogenic (60%), Trauma (20%), Spontaneous (15%)

Back 566

Treatment: If within 24 hours, can do primary repair with mediastinal drainage, NGT decompression, antibiotics. After 24 hours, exlusion and diversion.

Front 568

Achlasia

Back 569

Presentation: Dysphagia, regurgitation, weight loss.

Back 570

Etiology: Secondary to neural degeneration in muscle wall

Back 571

Diagnosis: Manometry (will show failure of LES to relax after food bolus, lack of peristalsis, increased LES resting pressure)

Back 572

Treatment: 1. Medical: Calcium channel blockers 2. Procedural: Dilatation, botulinum toxin injections. 3. Surgical: Heller myotomy (best, most long lasting effect) with partial fundoplication.

Front 574

Caustic esophageal injury

Back 575

Etiology: Injestion of alkalitic or acidic substances (alkalitic substances cause liquefaction necrosis and are deeper than injury caused by acids)

Back 576

Diagnosis:  Endoscopy to the level of injury.  If perforation is suspected to gastrograffin and then barium swallow.

Back 577

Treatment:  Depends on extent of injury.  For necrotic tissue or perforations, esophagectomy.  For hyperemia or ulcerations, conservative treatement with NPO, abx, IVFs.

Front 579

Esophageal Dysmotility

Back 580

Etiology: Associated with connective tissue disorders (SLE, Pliomyositis, Dermatomyositis, and Scleroderma)

Back 586

Esophagus

Front 590

Esophageal Cancer

Back 591

Epidemiology: Squamos Cell Carcinoma is most common histology worldwide (~95%). Adenocarcinoma is most common histology in U.S. (~60%).

Back 592

Presentation: Dysphagia, weight loss, difficulty swallowing solids. 70% will be non-resectable upon diagnosis.

Back 593

Prognosis: Average survival without esophagectomy is 6 months.

Back 594

Risk Factors: ETOH, tobacco, achalasia, nitrosamines (SCC). Tobacco, Barret’s esophagus (Adenocarcinoma). Barrett’s metaplasia raises risk 40x for adenocarcinoma.

Back 595

Indications for Surgery: High-grade Barret’s, and/or localized cancer.

Front 597

Leiomyoma

Back 598

Epidemiology: Most common benign tumor of the esophagus

Back 599

Presentation: Usually asymptomatic, but may cause dysphagia or retrosternal pressure/pain.

Back 600

Treatment: If symptomatic, or >5cm in size, submucosal enucleation.

Front 602

Zenker"s Diverticulum

Back 603

Etiology: Caused by increased pressure during swallowing. Occurs between thyropharyngeous and cricopharyngeous muscles.

Back 604

Presentation: May cause malnutrition or recurrent aspiration.

Back 605

Treatment: Cricopharyngeal myotomy with diverticulectomy.

Front 607

Epiphrenic Diverticulum

Back 608

Etiology: Esophageal dysmotility.

Back 609

Presentation: Can have dysphagia, regurgitation.

Back 610

Treatment: Diverticulectomy with long myotomy on opposite side of diverticulectomy.

Back 611

Etiology: Decreased lower esophageal sphincter tone.

Back 612

Treatment: Medical treatment first. If this fails, then fundoplication (over 80% success with this operation). Common cause of dysphagia after procedure is too tight of a wrap.

Front 614

Esophageal Perforation

Back 615

Presentation: Chest pain after forceful vomiting or iatrogenic after instrumentation.

Back 616

Etiology: Iatrogenic (60%), Trauma (20%), Spontaneous (15%)

Back 617

Treatment: If within 24 hours, can do primary repair with mediastinal drainage, NGT decompression, antibiotics. After 24 hours, exlusion and diversion.

Front 619

Achlasia

Back 620

Presentation: Dysphagia, regurgitation, weight loss.

Back 621

Etiology: Secondary to neural degeneration in muscle wall

Back 622

Diagnosis: Manometry (will show failure of LES to relax after food bolus, lack of peristalsis, increased LES resting pressure)

Back 623

Treatment: 1. Medical: Calcium channel blockers 2. Procedural: Dilatation, botulinum toxin injections. 3. Surgical: Heller myotomy (best, most long lasting effect) with partial fundoplication.

Front 625

Caustic esophageal injury

Back 626

Etiology: Injestion of alkalitic or acidic substances (alkalitic substances cause liquefaction necrosis and are deeper than injury caused by acids)

Back 627

Diagnosis:  Endoscopy to the level of injury.  If perforation is suspected to gastrograffin and then barium swallow.

Back 628

Treatment:  Depends on extent of injury.  For necrotic tissue or perforations, esophagectomy.  For hyperemia or ulcerations, conservative treatement with NPO, abx, IVFs.

Front 630

Esophageal Dysmotility

Back 631

Etiology: Associated with connective tissue disorders (SLE, Pliomyositis, Dermatomyositis, and Scleroderma)

Front 637

Treatment

Back 637

Transplant is only chance for long term cure. Endoluminal treatment can provide symptomatic relief, although this is usually temporary.

Front 638

Treatment

Back 638

Transplant is only chance for long term cure. Endoluminal treatment can provide symptomatic relief, although this is usually temporary.

Front 660

Hepatobiliary

Front 664

Physiology

Front 665

Hepatic biosynthesis

Back 665

albumin half life- 21 d, transferrin half life- 10 days, prealbumin- 2 days, Factor Vll shortest factor half life of 5-7 h.  Best indicator of liver funtion is PT.

Front 666

Drug Metabolism

Back 666

Cytochrome P450 - liver enzyme which metabolizes toxins and wastes - Phase I = oxidation, reduction, hydrolysis Phase II = conjugation

Front 667

Primary bile acids

Back 667

cholic acid and chenodeoxycholic acid Secondary bile acids

Front 668

Enterohepatic bile circulation

Back 668

bile salt pool= 2 gms and recycles 5-6 times/day. 0.5gms lost each day, and replaced by hepatic synthesis from cholestrol

Front 670

Inflammation/ Infection

Front 671

Hepatitis B- Anti-HepBsurface antibody (Anti-HBs) appears during the recovery phase of hepatitis at 2-16 weeks and helps eliminate active infection and protects against reinfection. Hep B vaccine is composed of recombinant HBsAg resulting in humoral production of anit-HBs and protection from possible future infections.

Front 673

Neoplasia

Front 674

Hepatic Hemangioma- do nothing unless giant or symptomatic/consumptive

Front 675

Hepatic Adenoma

Back 675

Prone to hemorrhage (1/3), usually solitary. Usually young women on OC. Rx

Front 676

Focal Nodular Hyperplasia

Back 676

Has central stellate scar.  Will take up sulfur colloid on technetium scan.  No malignancy risk.  No need for surgical resection.

Front 677

Hepatocellular CA

Back 677

Most common primary tumor of liver worldwide (mostly Asia and Africa). Risk factors

Front 679

Childs Classification For Liver Failure

Front 686

Advanced Surgical Recall (p464)

Front 687

Child-Pugh Criteria is slightly different

Back 687

Bilirubin, Albumin, PT (1-3, 4-6, >6), Ascites, and Neurologic disorder.

Front 688

Associated with mortality during venocaval shunt

Front 689

A - 7%, B-15%, C-33%

Front 691

Liver Abscess

Front 692

Etiology

Back 692

Pyogenic (most common), amebic, Echinococcal

Front 693

Diagnosis

Back 693

CT can usually differentiate between the three different kinds of abscess.

Front 694

Treatment

Back 694

Amebic (Flagyl), pyogenic (CT-guideded drainage and abx), echinococcal (preop albendazole followed by surgical excision)

Front 696

Gallbladder

Front 697

Complications

Back 697

  Shock within the first 24 hours most likely due to hemorrhage from bleeding cystic artery.  Shock after first 24hours most likely due to sepsis from inadvertant clipping of CBD.

Front 698

Cancer

Back 698

  Tumor that has not invaded into the muscularis propria can be treated with simple cholecystectomy, all others require radical resection.

Front 700

Sclerosing Cholangitits

Front 701

Etiolgy

Back 701

  Most likely autoimmune.  Can be associated with ulcerative colitis.

Front 702

Diagnosis

Back 702

  ERCP will show multiple strictures and dilations.  Patients blood can also be positive for Antimitochondrial antibodies.

Front 703

Treatment;  Transplant is only chance for long term cure.  Endoluminal treatment can provide symptomatic relief, although this is usually temporary.

Front 705

A

Front 706

B

Front 707

C

Front 708

Pancreas/Spleen

Front 712

Acute Pancreatitis

Front 713

Etiology

Back 713

Alcohol (most common), Biliary tract disease (e.g. gallstones), Hyperlipidemia, Hereditary, Trauma, Ischemia, etc. 10% idiopathic.

Front 714

Diagnosis

Back 714

H & P, Labs

Front 715

Amylase sensitivity

Back 715

70 to 90%

Front 716

Amylase + lipase sensitivity

Back 716

96%

Front 718

Ranson's Criteria

Front 719

Provides prognostic information to predict morbidity and mortality.

Front 720

Criteria on Admission

Front 721

Glucose>200, SGOT>250, LDH>350, Age>55, WBC>16,000

Front 722

Criteria after 48 hours

Front 723

HCT fall>10%, Base deficit <4mg, BUN increase>8mg, Serum Ca++<8mg, Arterial PO2<60mmHg, Fluid sequestration>6L

Front 724

Ranson Mortality Predictions

Front 725

<2 - 1% mortality

Front 726

2-4 - 16%

Front 727

>5 - 40%

Front 729

Pancreatic divisum

Front 730

Presentation

Back 730

Presents as pancreatitis of unknown etiology, no cancer, and very difficult ERCP canulation. Etiology

Front 731

Diagnosis

Back 731

ERCP

Front 732

Treatment

Back 732

stenting of minor papilla.

Front 734

Annular pancreas

Front 735

Presentation

Back 735

Presents as a GI obstruction, chronic pancreatitis, and/or peptic ulcers.

Front 736

Etiology

Back 736

Failure of normal clockwise rotation of ventral pancreas.

Front 737

Treatment

Back 737

duodenojejunostomy - no pancreatic resection.

Front 739

Pancreatic external fistula

Back 739

>7 days.

Front 740

>200 ml/day high output fistula

Front 741

< 200 ml/day low output fistula

Front 742

Common enteric fistulas in transverse colon or splenic flexure

Front 743

Treatment

Back 743

TPN, octreotide - most closes spontaneously.

Front 744

Surgical management

Back 744

roux en y to fistula. Also, whipple vs distal

Front 745

pancreatectomy, depending on where the fistula is.

Front 747

Whipple"s triad

Front 748

Hypoglycemic symptoms when fasting

Front 749

<50 mg/dl blood glucose

Front 750

Symptoms re with glucose

Front 752

Gallstone Pancreatitis

Front 753

Etiology

Back 753

The intramural portion of the distal common bile duct is shared with the pancreatic duct. Therefore, pancreatic duct hypertension may result when a gallstone obstructs the ampulla of Vater during passage into the duodenum leading to an acute pancreatitis. 3-8% of patients with symptomatic cholelithiasis develop gallstone pancreatitis.

Front 754

Treatment

Back 754

initially involves general supportive care with fluid resuscitation, early nutritional support, and hemodynamic and ventilatory support if indicated with the expectation that this cellular pathophysiologic process will be self-limited. Nasogastric drainage is useful in the presence of an ileus.

Front 755

Surgical Treatment

Back 755

Surgical therapy for pancreatitis is reserved for specific complications and for situations in which a correctable anatomic cause can be identified. The offending gallstone responsible for the pancreatitis will usually pass through the Sphincter of Oddi after the onset of pancreatitis. ERCP and sphincterotomy may be necessary to relieve the biliary obstruction. If pre-operative ultrasound documents choledocholithiasis, ERCP should be performed pre-operatively before laparoscopic cholecystectomy to decrease the necessity of laparoscopic common bile duct exploration. Regardless of whether ERCP is performed, intraoperative cholangiography is recommended if there is suspected or documented choledocholithiasis.

Front 756

Morbidity

Back 756

The rate of recurrent biliary pancreatitis is as high as 34 to 56% within 6 weeks. Therefore, cholecystectomy is often performed after the resolution of acute pancreatitis but before hospital discharge during the initial hospitalization.

Front 757

Norton. Surgical Decision Making, 2000.

Front 758

Greenfield, 2nd edition, pp 879-886

Front 760

Chronic Pancreatitis

Front 761

Recurrent bouts of pancreatitis with chronic pain.

Front 762

Etiology

Back 762

Alcohol most common cause (70%).

Front 763

Diagnosis

Back 763

CT findings include dilated pancreatic duct, calcification and atrophy of pancreas.

Front 765

Pancreatic Pseudocyst

Front 766

Etiology

Back 766

Arising from pancreatitis (20%) and trauma. Pancreatic fluid is enclosed within a false capsule of fibrous or granulation tissue.

Front 767

Treatment

Back 767

If infected, external drainage. For large uninfected cysts, internal drainage is preferred. Morbidity

Front 769

Gastrinoma

Front 770

Presentation

Back 770

Zollinger-Ellison Syndrome (ZES) consists of ulcer disease of the upper GI tract, marked increase in gastric acid secretion, and non-beta islet cell tumors. Gastrinomas are most common in the head of the pancreas and duodenum and may vary in size from 1 mm to more than 20cm in diameter. Ninety percent of sporadic gastrinomas are found in the “Gastrinoma Triangle” defined by

Front 771

#NAME?

Front 772

#NAME?

Front 773

#NAME?

Front 774

In unusual circumstances, ZES has resulted from gastrinomas originating in remote organs such as the parathyroids or ovaries. Sporadic gastrinomas are to be distinguished from MEN 1 syndrome, and autosomal dominant disorder with high degree of penetrance and highly variable expressivity. These patients usually present with multiple gastrinomas which are generally smaller and are located more frequently in the wall of the duodenum than in the pancreas.

Front 775

Diagnosis

Back 775

Ultrasound may be useful to detect small lesions deep within the substance of the pancreas and intraoperative endoscopy may be useful in transilluminating the duodenal wall as an aid in identifying small duodenal tumors. These tumors are often very small and in 1/3 of the patients are never identified at operation. Currently, Somatostatin Receptor Scintigraphy (SRS), also known as an octreotide uptake scan, is the initial imaging of choice once a diagnosis of ZES is established. This nuclear medicine study is limited only by the size of the tumor and not by location. Assistance with duodenal wall gastrinomas have been diagnosed with endoscopic ultrasound, SRS is believed to be equivalent to the combined modalities of angiography, ultrasound, MRI and CT.

Front 776

Cameron

Back 776

Current Surgical Therapy, 7th edition, pp 85-88

Front 777

Mastery of Surgery, 3rd edition, pp 544-546

Front 778

Schwartz, Principles of Surgery, 6th edition, pp 1428

Front 780

Pancreatic Lesion Associated with Watery Diarrhea

Front 781

Etiology

Back 781

VIP (vasoactive intestinal peptide is a 28 aa peptide that functions as a neuropeptide. VIP is a potent vasodilator, stimulates pancreatic and intestinal secretion, and inhibits gastric acid secretion. Symptoms of VIPoma include watery diarrhea, hypokalemia, and other achlorhydia or hypochlorydia, a syndrome termed WDHA syndrome or Verner-Morrison Syndrome. These can also cause metabolic acidosis and flushing.

Front 782

Presentation

Back 782

Patients typically have intermittent severe watery diarrhea averaging 5 L per day with a non-anion gap acidosis resulting from the loss of bicarbonate. The diagnosis is made after excluding other causes of diarrhea. This secretory diarrhea is refractive to bowel rest. Because VIP secretion is episodic, several levels should be obtained as one level cannot rule out disease.

Front 783

Diagnosis

Back 783

After biochemical documentation of VIP level, staging is done via dynamic abdominal CT with PO and IV contrast. In up to 10% of the cases, thoracic CT is necessary to identify extrapancreatic tumors in the thorax. MRI and arteriography may also be useful in the diagnosis. Octreoscan (Somatostatin receptor scintigraphy may also detect intra and extrapancreatic VIPomas.

Front 784

Treatment

Back 784

Surgical excision of VIPomas is appropriate in all cases with > 60% of VIPomas being malignant. VIPomas occur most commonly in the body or tail of the pancreas. Distal pancreatectomy is the operation for most VIPomas. These tumors are slow growing and debulking surgery with resection/ablation of liver mets may be indicated. If no tumor is found, the retroperitoneum and both adrenal should be evaluated. Medical treatment includes immediate administration of octreotide therapy to decrease the metabolic derangements. Long acting formulations such as Octreotide LAR and lanreotide are monthly or twice monthly injections. Streptozocin based chemotherapy has had modest responses. Other tumors such as ganglioneuroblastomas, mastocytomas, small cell carcinomas of the lung, pheochromocytomas, and GI carcinoids can also secrete VIP and account for 10% of VIP secreting tumors.

Front 785

Greenfield, 2nd ed, pp 925-926

Front 786

Scwartz. Endocrine Surgery, 2003

Front 787

Sabiston, 16th edition, 2001

Front 788

Harrison’s Principles of Internal Medicine, 13th edition, 1997

Front 790

Pancreatic Necrosis

Front 791

Presentation

Back 791

Septic complications related to pancreatitis should be suspected in patients with pancreatitis that fails to resolve in 7 to 10 days. Clinical findings of fever, tachycardia, abdominal pain, abdominal distention, and laboratory findings of hyperamylasemia, leukocytosis and bacteremia are characteristics of pancreatic necrosis (abscess).

Front 792

Diagnosis

Back 792

Abdominal films may identify retroperitoneal air described as “soap bubble sign”. The CT scan is the gold standard for non-invasive diagnosis of pancreatic necrosis with accuracy greater than 90%. CT san primarily delineates anatomy and complications. The finding though of peripancreatic fluid collections, pseudocysts, or peripancreatic necrosis is not an absolute indication for surgical treatment. Pancreatic necrosis with signs of sepsis should prompt aspiration. Confirmation is obtained with CT guided aspiration and identification of bacteria in the aspirate. The differentiation between inflammation and infection is essential.

Front 793

Treatment

Back 793

Without documented infection, aggressive nonoperative support is indicated. However in the presence of sepsis and infection, treatment requires broad spectrum antibiotic therapy (imipenem-cilastin) and prompt drainage. Percutaneous drainage techniques are usually ineffective due to thick, paste-like collections of infected necrotic tissue. Pancreatic necrosectomy is considered when septic physiology accompanies pancreatic necrosis. The mortality of severe peripancreatic necrosis can be reduced from 40% to 10% with aggressive surgical treatment. The two currently accepted alternatives for operative management of infected pancreatic necrosis/abscess are 1) laparotomy with debridement and wide sump drainage, and 2) laparotomy with debridement, open packing, and scheduled re-packing. Both techniques have comparable results. Pancreatectomy is rarely necessary in the treatment of severe pancreatitis. Norton. Surgical Decision Making, 2000

Front 794

Sabiston, 16th edition, p 1124

Front 796

Pancreatic Lymphoma

Front 797

Presentation

Back 797

Primary pancreatic (non-Hodgkin’s) lymphoma is rare. Symptoms of weight loss, jaundice, or palpable abdominal mass may be present.

Front 798

Diagnosis

Back 798

CT generally reveals a large soft tissue mass in the region of the pancreas with local lymphadenopathy. If pancreatic lymphoma is suspected, CT guided biopsy can confirm the diagnosis. Surgical intervention is reserved for cases where the needle biopsy is non-diagnostic but the suspicion for lymphoma remains high. After diagnosis is established, staging with bone marrow biopsy and CT of abdomen and chest should be done.

Front 799

Treatment

Back 799

Extensive surgical resection is not recommended. In patients with obstructive jaundice, temporary biliary decompression with an endoprosthesis or percutaneous transhepatic catheter may be necessary. Resections for stage I or II pancreatic lymphoma have been reported and have improved outcomes compared to ductal adenocarcinoma. Doxorubicin-based chemotherapy is used when no biliary obstruction is present. Long term remission can be obtained from chemotherapy alone.

Front 800

Sabiston, 16th edition, p 1139

Front 802

Periampulary Tumors

Front 803

Treatment

Back 803

If resectable, then Whipple and adjuvant 5 FU and 40 GY radiation

Front 804

If not resectable, chemoradiation , palliative bypasss, bile duct decompression.

Front 806

Pancreatic Carcinoma

Front 807

Prognosis

Back 807

90% dead in 1 year.

Front 808

Histopathology

Back 808

90% adenocarcinoma. 2/3 on the head of pancreas. Associated with Ca-19-9, Ca-50. Liver most common site of metastasis. K-Ras gene piont mutation in 80% of the cases.

Front 809

Treatment

Back 809

Whipple for resectable head of pancreas CA. If unresectable, then XRT and Chemo (5-fluorouracil).

Front 811

Palliative Treatment for Pancreatic Cancer

Front 812

Palliative treatment for cancer of the head of the pancreas is directed towards relief of obstructive jaundice, gastric outlet obstruction, and pain. In advanced disease, 70% of patients with pancreatic cancer will develop obstructive jaundice and 1/3rd of patients develop gastric outlet obstruction. Cholecystojejunostomy and choledochojejunostomy are both safe procedures of choice for relief of biliary obstruction. Gastrojejunostomy should be considered in patients who are expected to survive for more than a few months. Pain is a major symptom in up to 80% of patients with pancreatic cancer. The problem is best managed by chemical destruction of the celiac nerves and is achieved by percutaneous injection of 50% ethanol into the region of the ganglia under CT guidance. This can also be done at operation. Pain relief is possible in up to 80% of the patients. Although pain often recurs, repeated percutaneous injections can be performed with expected good results.

Front 813

Schartz, 7th edition, p 1491

Front 814

Esophageal Atresia (EA)/ Tracheoesophageal Fistula (TE)

Front 815

Presentation

Back 815

Feeding intolerance in neonate with or without coughing

Front 816

Classifications

Front 817

Type A

Back 817

EA without TE

Front 818

Type B

Back 818

EA with TE fistula b/w proximal esophogeal stump and trachea

Front 819

Type C

Back 819

EA with TE fistula b/w distal esophageal stump and trachea

Front 820

Type D

Back 820

EA with both proximal and distal TE

Front 821

Type E

Back 821

TE without EA (aka “H” type)

Front 822

Diagnosis

Back 822

EA

Front 823

Miscellaneous

Front 824

Most (30 – 50 percent) have associated abnormalities

Front 825

Type C is most common (85 to 90 percent)

Front 827

Pyloric Stenosis

Front 828

Presentation

Back 828

Nonbilious projectile vomiting, generally in children ages 4 to 8 weeks

Front 829

Electrolyte abnormality

Back 829

hypokalemic, hypochloremic metabolic alkalosis; may also demonstrate paradoxical aciduria

Front 830

Diagnosis

Back 830

olive on physical exam; ultrasound showing hypertrophic pylorus

Front 831

Treatment

Back 831

Resuscitate; pyloromyotomy

Front 833

Duodenal Atresia

Front 834

Presentation

Back 834

Bilious emesis in neonate

Front 835

DDx

Back 835

Malrotation with volvulus, annular pancreas (extrinsic obstruction), meconium ileus

Front 836

Diagnosis

Back 836

Double bubble sign on x-ray; GI series shows duodenum past midline

Front 837

Treatment

Back 837

Duodenoduodenostomy versus duodenotomy (for webs / windsock deformity); surgery deferred until all other systems are studied

Front 838

Miscellaneous

Back 838

Continuum including duodenal webs, stenosis, and atresia

Front 839

Most common cause of biliary emesis in neonate

Front 840

Associated with Down’s Syndrome, other anomalies

Front 841

Approximately 10 percent of obstructions are located before the ampulla (vomiting is not bilious)

Front 843

Biliary Atresia

Front 844

Presentation

Back 844

Unresolving jaundice in neonate

Front 845

Diagnosis

Back 845

Liver biopsy, HIDA scan, U/S

Front 846

Treatment

Back 846

Roux-en-Y hepaticojejunostomy (Kasai procedure); often requires OLT

Front 847

Miscellaneous

Back 847

Disease is exclusively extrahepatic in only 10 percent of cases

Front 848

Best results when surgery performed before 2 months of age; much less successful when performed after 3 months

Front 850

Choledochal Cysts

Front 851

Classification

Front 852

Type I

Back 852

solitary extrahepatic fusiform cyst (most common)

Front 853

Type II

Back 853

diverticulum of common bile duct

Front 854

Type III

Back 854

choledochocele

Front 855

Type IV

Back 855

Multiple intra- and extrahepatic cysts

Front 856

Type V

Back 856

Caroli’s Disease (diffuse intrahepatic cysts)

Front 857

Diagnosis

Back 857

U/S, ERCP, PTC

Front 858

Treatment

Back 858

Hepaticojejunostomy (type I); diverticulectomy (type II); excision / sphincteroplasty (type III); OLT (types IV & V)

Front 860

Malrotation

Front 861

Etiology

Back 861

Failure of complete rotation of midgut during embryologic development

Front 862

Classification

Back 862

Nonrotation, incomplete rotation, mesocolic hernia

Front 863

Diagnosis

Back 863

Upper GI series with oral contrast; duodenum crossing midline rules out diagnosis

Front 864

Treatment

Back 864

Emergent laparotomy for mid-gut volvulus with counterclockwise de-torsion, division of Ladd’s bands, appendectomy, placement of colon in left lower quadrant

Front 865

Miscellaneous

Back 865

Malrotation is associated with a short mesenteric axis, leading to volvulus and life-threatening mid-gut ischemia. Must be ruled-out in all children with bilious emesis

Front 867

Intestinal Atresia (Jejunal / Ileal)

Front 868

Etiology

Back 868

Intrauterine vascular accident; not failure of recanalization

Front 869

Presentation

Back 869

Polyhydramnios; bilious vomiting; abdominal distension

Front 870

Classifications

Front 871

Type I

Back 871

intraluminal diaphragm or web

Front 872

Type II

Back 872

Fibrous cord connecting two ends; mesentery intact

Front 873

Type IIIa

Back 873

Discontinuous bowel; V-shaped mesenteric defect

Front 874

Type IIIb

Back 874

apple core deformity

Front 875

Type IV

Back 875

multiple atretic segments

Front 876

Treatment

Back 876

Excision; multiple lesions in approximately 10 percent

Front 878

Meckel’s Diverticulum

Front 879

Etiology

Back 879

Remnant of omphalomesenteric duct on antimesenteric side of bowel

Front 880

Diagnosis

Back 880

Generally asymptomatic; commonly presents as source of occult GI bleeding in kids secondary to atrophic gastric tissue with mucosal ulceration; may also present as source of inflammation mimicking appendicitis

Front 881

Diagnosis

Back 881

Meckel’s scan for bleeding; generally found incidentally otherwise

Front 882

Miscellaneous

Back 882

Most common GI tract congenital abnormality

Front 883

Rule of two’s

Back 883

2 percent, two feet of ileocecal valve, two types of tissue (gastric, pancreatic), 2 percent symptomatic

Front 885

Ileocolic Intussusception

Front 886

Etiology

Back 886

Terminal ileum invaginates into colon; viral syndrome may precede onset of symptoms

Front 887

Presentation

Back 887

Colicky abdominal pain, bilious emesis, currant jelly stools, abdominal mass on physical exam

Front 888

Diagnosis

Back 888

Contrast enema

Front 889

Treatment

Back 889

Hydrostatic or pneumatic reduction; surgery for failure / recurrence

Front 891

Meconium Ileus

Front 892

Etiology

Back 892

Distal ileal obstruction secondary to thick, inspissated meconium

Front 893

Presentation

Back 893

Abdominal distension, bilious emesis, failure to pass meconium in a neonate

Front 894

Diagnosis

Back 894

Abdominal x-ray

Front 895

Treatment

Back 895

Generally non-operative (various enemas); surgery only if enemas unsuccessful

Front 896

Miscellaneous

Back 896

Associated with cystic fibrosis in 5 to 15 percent of cases

Front 898

Hirschsprung Disease (aka congenital aganglionosis coli)

Front 899

Presentation

Back 899

Bilious emesis, abdominal distension, constipation

Front 900

Diagnosis

Back 900

Barium enema, suction rectal biopsy (presence of ganglion cells rules out diagnosis)

Front 901

Treatment

Back 901

1. colostomy; 2. ileorectal anastomosis (various types); 3. colostomy takedown

Front 903

Necrotizing Enterocolitis (NEC)

Front 904

Etiology

Back 904

Unknown process leading to mucosal ischemia

Front 905

Presentation

Back 905

Nonspecific symptoms in a newborn after starting feeds, e.g., vomiting, abdominal distension, hematochezia

Front 906

Risk Factors

Back 906

Prematurity

Front 907

Diagnosis

Back 907

Largely clinical; pneumatosis intestinalis on x-ray

Front 908

Treatment

Back 908

Resuscitate, NPO, NGT, TPN, ABx, surgical resection of dead bowel

Front 910

Imperforate Anus

Front 911

Classification

Back 911

high (stump above puborectalis) versus low (stump below puborectalis)

Front 912

Treatment

Back 912

high

Front 913

Miscellaneous

Back 913

High lesions usually form fistulas either to prostatic urethra or vagina

Front 914

Low lesions usually with a fistula to perineum (scrotal raphe or vaginal fourchette); cases of imperforate anus in females are generally low

Front 916

Abdominal Wall Disorders

Front 917

Gastroschisis (bad bowel, good baby”)

Back 917

abdominal wall defect to right of umbilicus, without peritoneal sac. Rarely associated with other abnormalities. Treatment

Front 918

Omphalocele (“good bowel, bad baby”)

Back 918

abdominal wall defect; bowel hernia with peritoneal covering. Commonly associated with other abnormalities. Treatment

Front 919

Umbilical Hernia

Back 919

most close spontaneously; repair for defect greater than 2 cm, age > 2-3 years

Front 921

Congenital Diaphragmatic Hernia

Front 922

Presentation

Back 922

Respiratory distress, scaphoid abdomen in a neonate

Front 923

Diagnosis

Back 923

Fetal ultrasound, neonatal CXR for respiratory distress

Front 924

Treatment

Back 924

Intubation, NGT, ECMO as needed; transabdominal reduction, primary repair versus mesh

Front 925

Miscellaneous

Back 925

Most common on posterior lateral aspect of left side (Bochdalek)

Front 927

Inguinal Pathology

Front 928

Hernia

Back 928

patent process vaginalis; repair open versus laparoscopically

Front 929

Hydrocele

Back 929

fluid collection within scrotum; either communicating or non-communicating, depending on patency of process vaginalis. Non-communicating hydroceles tend to resolve spontaneously. Treatment via surgical evagination with repair of patent process vaginalis

Front 931

Syndromes

Front 932

VATER

Back 932

vertebral, imperforate anus, TE fistula, EA, renal abnormalites

Front 934

Pediatric Cancers

Front 935

Top three

Back 935

leukemia, brain tumor, neuroblastoma

Front 936

Neuroblastoma

Back 936

most common solid tumor in children <2 year of age

Front 937

Nephroblastoma (Wilms’)

Back 937

most common solid tumor in kids >2 y/oTeratomaMost common posterior mediastinal mass in children

Front 939

Pediatric Vital Signs

Front 940

BP HR

Front 941

Neonate 70/40 120-160

Front 942

3-12 months 90/50 90-140

Front 943

1-6 years 95/60 80-110

Front 944

6-12 years 100/70 70-100

Front 945

>12 years 120/70 60-90

Front 947

Pediatric Ages for Presentations

Front 948

Duodenal atresia

Back 948

neonates

Front 949

Meconium ileus

Back 949

neonates

Front 950

Malrotation with mid-gut volvulus

Back 950

first few weeks (50 percent)

Front 951

NEC

Back 951

first 2 weeks; premature infants

Front 952

Pyloric Stenosis

Back 952

4 to 8 weeks

Front 953

Intussusception

Back 953

5 to 10 month

Front 955

Pediatric Trauma

Front 956

Always consider abuse; distal aspect of little finger may be used to approximate size of trachea prior to intubation

Front 957

Skin Grafts

Front 958

Full thickness

Back 958

Contracts less, less likely to take, limited donor sites available

Front 959

Split thickness (STSG)

Back 959

More contraction, more likely to take, more available donor sites. STSG donor site heals from hair follicles and appendages

Front 960

Skin graft blood supply

Back 960

1st imbibition (diffusion from serum), then inosculation (capillary in-growth) in 2-7d

Front 962

Wound Healing

Front 963

Sequence of healing

Back 963

Platelets, neutrophils (24 hrs), macrophage, lymphocytes, fibroblasts (dominant by day 5)

Front 964

Collagen production

Back 964

Starts on day 3 and max in 3 weeks - then crosslinking for scar maturation and strength. Wound never stronger than pre-wound. Type III is replaced by type I in 3 weeks. Contraction by myofibroblasts.

Front 965

Collagen types

Front 966

I

Back 966

Most abundant overall. Bone, skin and tendon, scar

Front 967

II

Back 967

Cartilage

Front 968

III

Back 968

Embryonic tissue, blood vessels, uterus, GI. Low in Ehler Danlos syndrome

Front 969

IV

Back 969

Exclusively basement membrane

Front 970

Keloid - extends beyond margins of wound

Front 971

Hypertrophic scar - does not extend beyond boundaries of wound

Front 972

Vitamin A - helps with wound healing of patients on steroids

Front 973

Thromboxane A2

Back 973

platelet aggregation, vasoconstriction

Front 974

Prostacyclin

Back 974

platelet inhibition, vasodilation, bronchodilation

Front 975

Reopening a wound 5 days old results in quicker wound healing as cells and cytokines already in place

Front 977

Burn

Front 978

Classification

Front 979

1st degree

Back 979

erythema, pain. Sunburn.

Front 980

2nd degree

Back 980

blisters, pain.

Front 981

3rd degree

Back 981

Pain free (nerve endings burned), white/gray discoloration.

Front 982

Rule of 9s

Back 982

Used for estimating %TBSA burn. 9% each arm, 18% front trunk, 18% back trunk, 18% each leg, 9% head/neck, 1% perineum

Front 983

Hydrofluoric acid burn - treat with topical calcium gluconate

Front 984

Silvadene- risk of neutropenia, poor eschar penetration

Front 985

Sulfamylon-painful, can cause a metabolic acidosis (inhibits carbonic anhydrase)

Front 986

Silver nitrate- risk of hyponatremia and hypochloremia

Front 987

Parkland formula- Fluid resuscitation 4cc/kg/%BSA/24 hours. 50% given in 1st 8 hours, 50% over next 16 hours. Follow urine output.

Front 988

Burn pt with chest and extremity burns who has a sharp increase in peak pressure. Tx

Back 988

Escharotomy

Front 989

#1 Infection in burn patients is pneumonia

Front 991

Melanoma

Front 992

Risk Factors

Back 992

Dysplastic nevus, atypical nevus, or large congenital nevi. Xeroderma pigmentosum

Front 993

Types

Back 993

Superficial spreading (most common), Lentigo maligna, Nodular (most aggressive), Acral lentigus

Front 994

Treatment

Back 994

Resection with appropriate margins

Front 995

In situ

Back 995

0.5cm margin

Front 996

< 1mm

Back 996

1 cm margin

Front 997

1-4mm

Back 997

2 cm margin

Front 998

> 4mm

Back 998

Debated. 2cm most likely enough, some say 3cm.Nodes

Front 999

Gastric Lymphoma

Front 1000

Presentation

Back 1000

Occult bleeding, abdominal pain, ulcer type symptoms.

Front 1001

Pathology

Back 1001

Usually non-Hodgkin"s Lymphoma.

Front 1002

Diagnosis

Back 1002

EGD with biopsy

Front 1003

Treatment

Back 1003

Chemotherapy and radiation initially. Surgery is reserved for complications (e.g. obstruction).

Front 1005

MALT (mucosa associated lymphoid tissue)

Front 1006

Risk Factors

Back 1006

Is related to H.Pylori infection and is considered a precursor for lymphoma.

Front 1007

Treatment

Back 1007

Therapy for H.Pylori with triple antibiotics leads to regression of early-stage MALT in the majority of cases (75%). If no regression or advanced, chemotherapy and radiation. Surgery if complications arise (i.e obstruction).

Front 1009

Gastric Adenocarcinoma

Front 1010

Risk Factors

Back 1010

Adenoma >2cm, blood type A, pernicious/chronic atrophic gastritis, tobacco.

Front 1011

Diagnosis

Back 1011

EGD with biopsy

Front 1012

Treatment

Back 1012

Subtotal or total gastrectomy (should have 6cm resection margins)

Front 1014

Gastric Bypass

Front 1015

Eligibility

Back 1015

BMI >40 or BMI >35 with comorbidities.

Front 1016

Surgery

Back 1016

Operative mortality is ~1%, HTN, NIDDM and sleep apnea often resolve after surgery.

Front 1017

Roux-en-Y gastric bypass

Back 1017

Better weight loss than with stapling

Front 1018

Perioperative complications

Back 1018

Ischemia, leading to anastamotic leak, marginal ulcers, anastomotic stenosis, infection. 6 months post-gastric bypass presenting with abdominal pain - consider cholecystitis and marginal ulcer

Front 1020

Gastric Ulcer Disease

Front 1021

Etiology

Back 1021

ETOH, NSAIDS, H. pylori, uremia.

Front 1022

Presentation

Back 1022

Epigastric pain radiating to the back, which is relieved with eating but recurs 30 minutes after.

Front 1023

Diagnosis

Back 1023

H. pylori serlogy test of choice when endoscopy is not required. If endoscopy, do a CLO test - detects urease activity in H. pylori. Biopsy must be taken from antrum.

Front 1024

Treatment

Back 1024

H2 blockers or proton pump inhibitors. Triple therapy with antibiotics for those that are H.Pylori positive. Urea breath test 4 weeks after treatment completed, if necessary to confirm eradication. Surgery if indicated.

Front 1025

Indications for surgery

Back 1025

Perforation, bleeding, obstruction, unable to exclude malignancy, intractability (>3 months without relief with medical treatment or 2nd recurrence)

Front 1026

Type I ulcer- on the lesser curve of stomach. Associated with blood type A

Front 1027

Type II ulcer- lesser curve and duodenal ulcers

Front 1028

Type III ulcer- pre-pyloric

Front 1029

Type IV ulcer- high on the lesser curve

Front 1030

Type V ulcer- any location, but associated with NSAID use

Front 1032

Carcinoid Tumors

Front 1033

Etiology

Back 1033

Arise from neuoroendocrine cells.

Front 1034

Incidence

Back 1034

Appendix>Ileum>Rectum

Front 1035

Ileal carcinoid has highest propensity for metastasis

Front 1036

33% of patients with carcinoid have multiple primary sites

Front 1037

25% of patients with carcinoid have metachronous adenocarcinoma

Front 1038

Diagnosis

Back 1038

Most appendiceal carcinoids are diagnosed on pathology after appendectomy. If symptoms of carcinoid syndrome are present, can do a I123 labeled Octreotide scan. Detection of urinary 5 HIAA can aid in diagnosis.

Front 1039

Appendiceal carcinoids

Back 1039

Most common site for carcinoic tumor (50%)

Front 1040

Presentation

Back 1040

Usually an incidental finding after appendectomy

Front 1041

Treatment

Back 1041

If >2cm and/or involving the base of the appendix --> right hemicolectomy, otherwise, appendectomy is sufficient

Front 1042

Small bowel carcinoids

Back 1042

Patients are at increased risk for multiple primaries and secondary unrelated malignancies.

Front 1043

Presentation

Back 1043

Usually as SBO

Front 1044

Treatment

Back 1044

Segmental resection

Front 1045

Rectal carcinoids

Back 1045

Most common site for carcinoid syndrome

Front 1046

Presentation

Back 1046

Usually as partial obstruction

Front 1047

Treatment

Back 1047

<2cm wide local excision, >2cm or invasion of muscularis propria, do an APR

Front 1048

Gastric Carcinoid

Back 1048

Uncommon location for carcinoid tumors

Front 1049

Presentation

Back 1049

Usually as abdominal pain

Front 1050

Treatment

Back 1050

If <1cm can do endoscopic excision. If >1 cm, subtotal gastrectomy and omentectomy.

Front 1052

Carcinoid Syndrome

Front 1053

Presentation

Back 1053

Flushing, diarrhea, asthma, valvular insufficiency, crampy abdominal pain, borborygmi.

Front 1054

Etiology

Back 1054

Happens when venous drainage of carcinoid tumors escapes hepatic metabolims of seretonin. Functioning carcinoid tumors divert 60% of tryptophan to produce seretonin. Serotonin is secreted by argentaffin staining cells (eterochromaffin cells). 9% of patients with metastatic disease get carcinoid syndrome. May treat with octreotide.

Front 1055

Diagnosis

Back 1055

If location of primary tumor unkown, can do a I123 labeled Octreotide scan. Detection of urinary 5HIAA can aid in diagnosis.

Front 1056

Treatment

Back 1056

Octreotide

Front 1058

Crohn’s Disease

Front 1059

Presentation

Back 1059

Intermittent abdominal pain, weight loss, and diarrhea. Can have extraintestinal manifestations (arthritis, arthralgias, erythena nodosum, pyoderma gangenosum, ocular diseases). Termainal bowel is the most commonly involved bowel segment

Front 1060

Diagnosis

Back 1060

Colonosocopy with biopsies

Front 1061

Treatment

Back 1061

Medical, 5-ASA, sulfasalazine, steroids, Remicade. TPN if fistula is present. Surgery if indications present.

Front 1062

Surgical indications

Back 1062

Obstruction (if not resolved with medical treatment), Hemorrhage, Megacolon. Patients often have numerous strictures. Avoid resection if possible, because extensive resection can lead to short gut.Perform stricturoplasties if possible. Duodenal stricture tx

Front 1064

Small Bowel Obstruction (SBO)

Front 1065

Etiology

Back 1065

Most common cause is adhesions from previous abdominal surgery. Without history of surgery, hernia is most common cause

Front 1066

Treatment

Back 1066

Bowel rest and NG tube decompression cures 65% of partial SBO. Bowel rest and NG tube decompression cures 20% of complete SBO. Surgery with exploratory laparotomy for those that don"t resolve with conservative treatment, or with signs of strangulation or perforation.

Front 1068

Gallstone Ileus

Front 1069

Presentation

Back 1069

Usually an elderly patient (>70 yo). with signs of intermittent SBO.

Front 1070

Etiology

Back 1070

cholecysto-enteric fistula.

Front 1071

Diagnosis

Back 1071

Small bowel obstruction with air in the biliary tree.

Front 1072

Treatment

Back 1072

Remove stone to relieve obstruction with ex. lap. and enterotomy. Most will leave gall bladder and fistula intact to decrease mortality

Front 1073

Thoracic viceral afferent nerves mediate pain from small intestines

Front 1075

Post-ERCP acute abdomen or shock - Get CXR, KUB, and Gastrograffin swallow study. Rule out retroduodenal perforation which occurs in 1% or ERCP.

Front 1077

Omphalocele - defective closure of umbilical ring. Viscera with covering

Front 1079

Gastroschisis - abdominal defect lateral to umbilicus. No visceral covering.

Front 1081

Meckel"s diverticulum

Front 1082

Etiology

Back 1082

derivative of vitelline duct.

Front 1083

Presentation

Back 1083

found in adults incidentally during laparotomy. In children can cause painless rectal bleeding 2/2 peptic ulceration for ectopic gastric mucosa.

Front 1084

Diagnosis

Back 1084

Tc 99m-pertechnetate radioisotope scintiscan. Lights up parietal cells.

Front 1086

Resection of the Terminal Ileum

Front 1087

Complications

Back 1087

Leads to decreased bile salt absorption, which leads to less colonic water absorption, and diarrhea. Decrease intrinsic factor absorption, and thus vitamine B12 deficiency, Decreased binding of oxalate leads to more oxalate absorbed in the colon, and thus urinary oxalate stones and gallstones.

Front 1088

Post-Transplant rejections

Front 1089

Hyperacute rejection - minutes to hours mediated by preformed antibodies - prevent by crossmatching, not meds

Front 1090

Acute rejection - 1-3 weeks, mediated by T-lymphocyte - treat with OKT3

Front 1091

Chronic rejection - months to years, loss of blood supply - no treatment

Front 1093

Transplant Meds

Front 1094

FK506 - inhibits IL-2 expression in T-cells

Front 1095

Prednisone - inhibits IL-1 expression in macrophages

Front 1096

Cellcept (mycophenolate) - attentuates T and B cell proliferation by inhibiting purine synthesis

Front 1097

Cyclosporin - inhibits IL-2 expression (remember nephrotoxicity)

Front 1098

OKT3 - monoclonal Aby, treate acute rejection

Front 1100

Immunology Basics

Front 1101

Innate immune system

Back 1101

recognizes general classes of antigens that have become universal pathogens during human evolution. Complement plays a central role.

Front 1102

Alternative pathway

Back 1102

is activated by carbohydrates lacking sialic acid (sugar moiety found in most human cells). C3 is cleaved resulting in byproducts that form a MAC (membrane attack complex) and recruit lymphocytes.

Front 1103

Classical pathway

Back 1103

involves antigen-bound antibody binding with complement C1q which activates C3. Macrophages and dendritic cells engulf cells bound by complement.

Front 1104

Acquired immunity

Back 1104

involves a specific and acquired recognition of pathogens.

Front 1105

T-cell formation

Back 1105

T cells are formed in fetal liver/bone marrow and migrate to thymus for development. T cells undergo thymic selection, first by allowing cells that recognize self-MHC to survive (positive selection). Survivors that bind to self-MHC with too high of affinity undergo apoptosis (programmed cell death), called negative selection. T cell activation involves interaction between the T cell and MHC of self-cells. Activation also requires accessory molecules (CD4 and CD8) that improve TCR binding affinity. CD8 expressing T cells interact with Class I MHC molecules (parenchymal cells of the body). CD4 expressing T cells interact with Class II MHC molecules (antigen presenting cells).

Front 1106

CD8 T Cells

Back 1106

mediate cytotoxicity. Killing of cells with Class I MHC molecules (with appropriate antigen) occurs via calcium dependent release of perforins and granzymes or calcium independent induction of apoptosis within the target cell. B cells are responsible for the antibody mediated immune response. B cell maturation occurs in the bone marrow.

Front 1107

Immunoglobulin Antibodies

Back 1107

Five main classes of heavy chains exist, which define the Ig type as IgM, IgG, IgA, IgE, or IgD. Once activated, B cells undergo isotype switching changing initial antibodies from the IgM type to another heavy chain type. B cells recognize antigen via antibodies. When antigen is bound, the antibodies crosslink on the cell surface which stimulates activation, proliferation, and differentiation of that particular B Cell line. Antibody dependent cellular cytotoxicity occurs when antibody bound to antigen interacts with C1q of the classical complement pathway, leading to destruction of the target cell. Cytokines are soluble mediators of cell-cell communication that facilitate the amplification of a specific immune response.

Front 1108

Th1 T cells (cells that mediate the cytotoxic response) express IL2, IL12, IL 15, and IFN gamma. Th2 T cells (cells that mediate humoral or eosinophilic responses) often secrete IL4, IL5, IL10, and IL13.

Front 1110

Transplant Immunity

Front 1111

Antigens primarily responsible for graft rejection include Class I molecules (HLA A,B,C) and Class II molecules (HLA DR, DP, and DQ). Even those identical in these classes still can undergo rejection based on minor HLA gene differences.

Front 1112

Class I molecules

Back 1112

are found mainly on parenchymal cells.

Front 1113

Class II molecules

Back 1113

are found mainly on antigen presenting cells.

Front 1114

HLA inheritance

Back 1114

is Mendelian. T cells with CD8 bind to Class I molecules and CD4 cells binds to class II molecules.

Front 1115

MHC matching is determined via two assays

Back 1115

the lymphocytotoxicity assay and the MLC. Class I is now tested for by lymphocytotoxicity assay while class II is usually done with PCR. HLA matching clearly improves outcome of kidney, heart, and pancreas transplantation, but not liver transplantation

Front 1117

T Cell vs Antibody Mediated Rejection

Front 1118

T cells

Back 1118

are the primary mediators of acute allograft rejection. T cells can respond to transplant antigens via binding to foreign MHC molecules or via self APC’s that have presented alloantigens on self MHC molecules. Initial binding occurs between recipient T cells and donor endothelium or APCs, mediated by costimulatory signals which are upregulated following surgical trauma and ischemia. Once T cell activation occurs IL2 and IFN gamma recruit other T cells and potentiate clonal expansion. Late in the process of rejection, the inflammatory response recruits cells with nonspecific cytotoxic activity to the organ.

Front 1119

Antibody responses

Back 1119

by the host vs the graft also accompanies the primary T cell response in acute rejection. In hyperacute rejection and acute vascular rejection, antibodies are the primary mediator.

Front 1121

Clinical Rejection

Front 1122

Hyperacute rejection occurs when donor specific antibodies are present in the recipient’s serum prior to transplantation. Recipient antibodies bind to donor tissue mediating endothelial cell activation, a procoagulant state and immediate graft thrombosis. There is no treatment other than removal of organ.

Front 1123

Vascular rejection is a delayed variant of HAR. It occurs when alloantibodies exist in a recipient’s serum at levels undetectable by a crossmatch assay. Result is initial graft function with rapid deterioration at POD 3. Treatment is enhanced immunosuppresion with steroids, plasmapharesis, or nonspecific immunoglobulin administration.

Front 1124

Acute rejection can occur after POD 4 and most commonly before 6 months posttransplant. Occurs over days to weeks, with a massive infiltration of T cells (both CD4 and CD8) within the graft and resulting destruction/thrombosis. Tx is prompt recognition and enhanced immunospurression. Acute rejection is often detected only after graft is rendered non-functional. Thus, montiroring for acute rejection should occur in the first year. Prevention is usually with a calcineurin inhibitor (Cyclosporin or Tacrolimus) and corticosteroids, with frequent addition of MMF or azathioprine. 10-40% of transplant recipients experience rejection in the first several weeks. High dose steroids are the most common drugs used for rescue. 75% resolve with pulse steroid therapy. OKT3 arrests 100% of all rejection episodes.

Front 1125

Chronic rejection is poorly understood. Appears due to gradual loss of blood supply. Insidious and occurring over months to years, it is untreatable. Graft vs host desiase is mediated by T cells.

Front 1127

Immunosuppresion

Front 1128

Side Effects

Back 1128

All immunosuppresion puts the recipient at increased risk for infection or malignancy. More viral than bacterial infections. Cancers increased

Front 1129

Induction immunosuppression is the intense immunosuppression used in the early postop period, involving complete shutdown of T cell response.

Front 1130

Maintenance immunosuppressants are designed to prevent acute rejection for the life of the patient.

Front 1131

Rescue immunosuppressants are used to reverse an acute rejection episode, and generally are the same agents used for induction therapy.

Front 1132

Corticosteroids used with other agents significantly improve graft survival. Glucocoritcosteroids bind to an intracellular receptor after nonspecific uptake into the cytoplasm. The receptor-ligand complex acts as a DNA binding protein and increases transcription of several gene the most important is IkappaBalpha which binds to NfkappaB an activotor of proinflammatory cytokines and transcription factor for Tcell activation. They also mute MHC upregulation and IFNgamma production. Most common is prednisone or methylprednisolone.

Front 1133

Azathioprine

Back 1133

is an antiproliferative agent. Aza undergoes hepatic conversion to 6-MP then 6 tIMP which both inhibit DNA synthess by alkylating DNA precursors and inducing chromosomal breaks. It all acts on all rapidly deviding cell with toxicity to bone marrow, gut mucosa, and liver.

Front 1134

Mycophenolate mofetil (MMF)

Back 1134

is a noncompetitive reversible inhibitor of IMP dehydrogenase. IMP dehydrogenase is key in synthesis of GMP a precuros of RNA and DNA. Most cells have a salvage pathway, except lymphocytes. Decreases T and B cells.

Front 1135

Cyclosporine

Back 1135

is a calcineurin inhibitor and is specific for T cells. CyA binding with cyclophilin creates a complex which binds to calcineurin/calmodulin, blocking the activation of transcription factor NF-AT, preventing transcription of IL2. CyA also increases TGF-beta transcription which downregulates T cells. Solely a maintenance agent. Metabolized by P450 system. Decreases renal blood flow by 30%. Promotes fibrosis. Increases hypertension. Hyperkaliemia may results. Hypertrichosis 50%. Gingival hyperplasia.

Front 1136

Tacrolimus (FK506) blocks NF-AT preventing cytokine transcription and arrests T cell activation. The target of tacrolimus is FK-BP. Side effects are similar to CyA. Neurotoxicity is more pronounced. Has become the drug of choice.

Front 1137

ALG (Antilymphocyte globulin) is a polyclonal antibody preparation containing antibodies directed against many antigens on lymphocytes. Can be used as an induction or rescue agaent. Most prominent side effect is severe thrombocytopenia,. Other SE’s include fever/chills (20%), rash.

Front 1138

OKT3 is a monoclonal antibody is directed at CD3 a signal transduction unit on T cells. Binding of OKT3 to CD3 leads to internalization of the TCR. Administration of OKT3 can lead to profound systemic cytokine release syndrome resulting in hypotension, pulmonary edema, and fatal cardiac myodepression. 2% of pts have aseptic meningeal inflammation. Administration of methylprednisolone is required before OKT3. Often used as a rescue or induction.

Front 1139

Anti IL-2 agents

Back 1139

are directed against CD25 (part of the IL2 receptor).

Front 1140

Rapamycin is a macrolide antibiotic. Similar to tacroliumus, it interacts with FK-BP but does not affect calcinuerin, thus having no effect on NF-AT or IL2 expression. Rather, it impairs signal transduction by the IL2 receptor, arresting the cell before S phase of the cell cycle.

Front 1142

Kidney Transplantation

Front 1143

Indications

Back 1143

A pt with ESRD from any cause. Range 1 to 70. Free of infx and ca for 5 yrs.

Front 1144

Procedure

Back 1144

Heterotopic graft placed in the extraperitoneal iliac fossa. Renal a and v sewn to iliac vessels and uriter implanted into urinary bladder. Acute rejection signs/symptoms

Front 1145

Complications

Back 1145

Early – excessive diuresis, urinary leak/fistula, hemorrhage, vascular anastomotic leak, thrombobis, formation of perigraft lymphocele, graft rupture, sevre rejection. Late – stenosis of ureter or renal artery, recurrent primary renal disease, neoplasia.

Front 1146

Prognosis

Back 1146

Functional graft survival at one year is 75-85% for cadaveric and 95% for living related at 1 year. Pt survival is 95% at 1 year.

Front 1148

Liver Transplantation

Front 1149

Indications

Back 1149

Life expectancy of 1 year or less. Free of malignancy or infection. Proven benefit with Cirrhosis, PBC, PSC, Metabolic, Congenital biliary atresia, congenital hepatic fibrosis. Possible benefit with acute liver failure, Budd chiari, Rare primary hepatic tumor. Questionable benefit with HCC, Mets, Alchoholic hepatitis

Front 1150

Procedure

Back 1150

Removal of recipient native liver begins while donor liver is being removed. After native hepatectomy completed, new liver is implanted by sewing the suprahepatic vena cava to the cuff of the remaining suprahepatic vena cava and performing an infrahepatic vena caval anastamosis. Donor hepatic artery connected, as is the portal vein. Biliary drainage achieved with primary anastamosis in adult and roux-en-y choledochojejunostomy inc hild.

Front 1151

Complications

Back 1151

Early - Perioperative hemorrhage, Bleeding disorders, Vascular thrombosis, Biliary tract leaks/strictures, Acute rejection is less common and milder than kidney. Late - Biliary tree stenosis, recurrent hepatitis, ongoing chronic rejection, CyA toxicity. If biliary stricture post transplant is suspected, arterial flow should be checked as this may be due to ischemia.

Front 1152

Prognosis

Back 1152

85% graft survival at 1 year.

Front 1156

Heart Transplantation

Front 1157

Indication

Back 1157

End stage cardiac failure expected to die within 6 mos. Free of infection/neoplasm, Hypertensive/Idiopathic/viral/ischemic/postpartum cardiomyopathy, or Terminal valvular disease

Front 1158

Procedure

Back 1158

Size matched. Donor heart sewn by attaching left and right atria of the donor to the left and right atria of the recipient. Pulmonary a and aortic a anastomoses are completed.

Front 1159

Complications

Back 1159

Early – infection, rejction with cardiac failure, cva. Late – chornic rejection, accelerated CAD.

Front 1160

Prognosis

Back 1160

1 year graft and pt survival is 80% or higher, 5 year is 60-70%

Front 1162

Heart-Lung Transplantation

Front 1163

Performed when pulmonary hypertesnion accompanies cardiac dx. Also with congenital heart dx. Complications include restrictive fibrosis of the lung. 1 yr survival rate is 63%.

Front 1165

Lung Transplantation

Front 1166

Indications

Back 1166

Alpha 1 antitrypsin deficiency, Interstial pulmonary fibrosis, Primary pulmonary hypertension, Cystic fibrosis, Emphysema

Front 1167

Contraindication

Back 1167

Lung cancer and/or >65 years old

Front 1168

Complications

Back 1168

Rejection – dx’d with infiltrates on xray and confirmed by endoscopy and bx. Anastamotic breakdown occurs in 5% of transplants.

Front 1169

Procedure

Back 1169

Postlateral thoracotomy for single lung and transverse thoracotomy for double lung. Pulmonary vv are seewn to left atrial receipient cuff aft ersleeve bronchial anastomaosis is performed. Pulmonary aa are then anastamosed.

Front 1170

Prognosis

Back 1170

73% at 1 year and 57% at 3 years

Front 1172

Pancreas/Islet Transplantation

Front 1173

Indications

Back 1173

Type I DM

Front 1174

Procedure

Back 1174

Donor pancreas and duodenal C sweep are transplanted together in the false pelvis of the recipient, intraperitoneally. Donor arteries are anastamosed to iliac a. Donor veins are anastomosed to the iliac vein. Duodenal sweep is attached to the dome of the bladder. Pancreatic function monitored by amylase in urine.

Front 1175

Complications

Back 1175

Increased rejection, More infections, Anastamotic leak, vascular thrombosis, urinary complications

Front 1176

Prognosis

Back 1176

80-95% survival.

Front 1178

Intestinal Transplantation

Front 1179

Indications

Back 1179

Short gut syndrome, Crohn’s, Low grade tumors, Necrotizing enterocolitis

Front 1180

Procedure

Back 1180

SB at least 100-150cm long is necessary.

Front 1181

Complciations

Back 1181

Sepsis from bacterial translocation

Front 1182

Prognosis

Back 1182

Less than 3 year (mostly one) graft survival.

Front 1183

Tension Pneumothorax

Front 1184

Presentation

Back 1184

Acutely ill, hypotension, hypoxia, tachycardia, absent or decreased breath sounds, and tracheal shift away from the affected side.

Front 1185

Diagnosis

Back 1185

clinical presentation (not Xray) as above.

Front 1186

Treatment

Back 1186

immediate decompression and restoration of respiratory capacity. An 18 gauge needle can be inserted into the second intercostal space, mid-clavicular line to decompress the pneumothorax. This is immediately followed by closed chest tube drainage from an anterior or lateral chest tube. There is usually an immediate response to therapy with return of blood pressure and decreased respiratory distress.

Front 1188

Parasternal Stab Wound

Front 1189

Presentation

Back 1189

Stab wound, hypotension, SOB

Front 1190

Diagnosis

Back 1190

portable CXR, EKG. If anterior to anterior axillary line and below 5th intercostal, then FAST or DPL.

Front 1191

Treatment

Back 1191

  If hemo or pneumo, place chest tube - no wound exploration. Emergent thoracotomies if 1) pericardial tamponade 2) hemothorax greater than 1.5 liter initially or sustained hemorrhage more than 250 cc/hrx4hrs, and 3) hypovolemic shock. Left anterolateral thoracotomy gives best exposure to heart, great vessels, descending aorta and pulmonary structures. "Book" or "trap door" incision for exposure of long segments of left subclavian or carotid.

Front 1193

Duodenal Hematoma

Front 1194

Presentation

Back 1194

Blunt abdominal trauma. Nausea, vomiting, upper abdominal pain, right upper quadrant mass on palpation

Front 1195

Diagnosis

Back 1195

  upper GI is usually diagnostic with filling of the duodenal lumen and the appearance of a "coiled spring" in the second and third portions due to crowding of the valvulae conniventes. Elevated amylase.

Front 1196

Treatment

Back 1196

  cessation of oral intake, nasogastric suction, and intravenous replacement of fluids and electrolytes. If no improvement >7 days, then operate for drainage of hematoma.

Front 1198

Blunt Thoraci Vascular Trauma

Front 1199

Mechanism

Back 1199

deceleration (MVA, fall) with shear force between mobile and fixed segments - ligamentum arteriosum. Tear just distal to left subclavian takeoff. 85% mortality before reaching hospital.

Front 1201

Characteristics of Cerebral Perfusion Pressure

Front 1202

Cerebral Perfusion Pressure (CPP)=MAP-ICP

Front 1203

MAP=mean arterial pressure

Front 1204

ICP=intracranial pressure

Front 1205

Normal CPP=80-100 mmHg

Front 1206

Decreased CCP occurs with elevated ICP or decreased systemic arterial blood pressure Cerebral blood flow decreases rapidly when the CPP<60 mmHg, potentially imposing an additional ischemic-hypoxic injury on the mechanical traumatic injury. Therapy is designed to maintain CPP>60 mmHg

Front 1208

Pelvic Fractures

Front 1209

High-energy trauma e.g. MVA. Large amount of bleeding into pelvis and retroperitoneum. If in shock without other sources of blood loss and does not respond to standard volume replacement therapy, application of an anterior external fixator to stop bleeding. Angiography and intraarterial embolization my be necessary to control continued bleeding from disrupted pelvic vessels. Overall the majority of pelvic fractures can be treated without surgical intervention. Sacral and coccygeal fractures are generally treated symptomatically.

Front 1211

Femoral Fracuture

Front 1212

Treatment

Back 1212

stabilization with a splint or traction splint. Intramedullary (IM) rod fixation is now the standard method of treatment. IM rod fixation facilitates mobilization of the patient within 24 hr, an important factor in managing any trauma patient.

Front 1213

In adults with medical contraindications to surgery, traction until callus formation and a cast brace or hip spica cast may be appropriate. If signs of distal ischemia are present, arteriography is indicated.

Front 1214

Children - treated conservatively with distal femoral skeleton traction. Open Femoral fx - Goal

Back 1214

prevention of infection. Tx

Front 1216

Traumatic Pericardial Tamponade

Front 1217

Mechanism

Back 1217

It is usually caused by penetrating thoracic injuries but can also be caused by blunt trauma-myocardial rupture, coronary artery laceration, or ascending dissection of an aortic tear.

Front 1218

Presentation

Back 1218

  Beck"s classic triad of distended neck veins, shock and cyanosis is seen in only 1/3 of patients and pulsus paradoxus is even less discernible. The symptoms of cardiac tamponade can take up to 2 hours to develop. Other symptoms include increased venous pressure, decreased pulse pressure, paradoxical pulse +/- cyanosis and decreased heart

Front 1220

Fluid Resucitation of Burn Patients

Front 1221

Parkland Formula

Back 1221

4 mL/kg/%TBSA burned. Half is given in the first 8 hours post burn and the second half is given in the next 16 hours.

Front 1222

Bolus to be avoided. Urinary output most reliable index - kidneys most poorly perfused organ in the burn patient. Urine flow goal

Back 1222

0.5 mL/kg in an adult and 1.0 mL/kg in a child up to 30 kg.

Front 1223

Electrical burns with myoglobinuria require urinary outputs of 100-150 mL/hr with the possible addition of sodium bicarbonate (urinary alkalosis with a pH >5.6 increases solubility of myoglobin) and mannitol (osmotic diuretic). During the second 24 hours, dextrose/free water (D5W) and colloid (0.5mL/kg?% burn, usually as 5% albumin in NS) are added.

Front 1224

Compartment Syndrome

Front 1225

Presentation

Back 1225

Anterior compartment of leg most susceptible to compartment syndrome...contains deep peroneal nerve...foot drop with injury; first toe webspace numbness is usually first symptom (other than PAIN) of anterior compartment syndrome.

Front 1226

Diagnosis

Back 1226

Intra-compartment pressure of greater than 30 mmHG highly concerning for compartment syndrome; greater than 40 is unquestionably positive. Other compartments are lateral, superficial posterior, and deep posterior. On physical exam, pain with passive extension of the muscle group in the involved compartment is the most sensitive finding to dx compartment syndrome

Front 1228

Most common peripheral aneurysm

Back 1228

popliteal aneurysm. 50% bilateral 75% have aneurysm elsewhere. Repair if embolic or >2cm. Emboli is most common clinical manifestation. Operative treatment is exclusion and bypass.

Front 1230

Most common visceral aneurysm

Back 1230

splenic a. aneurysm Repair if >2cm, symptomatic, or child bearing age

Front 1232

Vein graft failures

Front 1233

Early

Back 1233

- thrombosis, secondary to technical errors

Front 1234

Late

Back 1234

- atherosclerotic progression/fibrointimal hyperplasia

Front 1235

Cutaneous signs of thrombosed arteries

Back 1235

Demarcation occurs approximately 10 cm distal to site of thombosis on the limb

Front 1237

Reperfusion Injury

Back 1237

Following re-establishment of arterial inflow following an ischemic event. Leaky capillaries and free oxygen radical induced cell membrane dysfuncion lead to profound edema and compartment syndrome necessitating fasciotomy. Commonly seen following lower extremity embolectomy with below knee four compartment faciotomy needed.

Front 1239

Carotid Disease

Front 1240

Stroke Risk

Front 1241

#NAME?

Back 1241

CEA decreases 5yr stroke rate from 11% to 5%.

Front 1242

-Symptomatic with stenosis >70% (NASCET Study)

Back 1242

CEA reduces 5yr stroke rate from 26% to 9%.

Front 1243

#NAME?

Front 1244

Pseudoaneurysm post CEA

Back 1244

typically seen at 6 months post op

Front 1245

Diagnosis

Back 1245

with duplex

Front 1246

Treatment

Back 1246

surgery (repair vs. patch vs. exclusion and bypass).

Front 1247

Amaurosis fugax is temorary unilateral vision loss with "shade going down on my eye" phenomenon; due to atheroemboli to ophthalmic artery (first intra-cranial branch of ICA).

Front 1248

Carotid bulb is a baro-receptor, stimultion causes parasympathetic response (bradycardia and vasodilation).Carotid sinus is a chemoreceptor, detects CO2/acidosis and causes sympathetic response.

Front 1249

Vagus is the most commonly injured nerve during CEA, results in unilateral vocal cord paralysis (hoarseness)

Front 1250

Sequence of opening circulation after CEA

Back 1250

common carotid, external carotid, internal carotid.

Front 1252

Abdominal Aortic Aneurysm

Front 1254

repair if greater than 5.5cm.

Front 1255

Pathophysiology include decrease TIMP1 and 2 and increase in MMP1 and 9, IL1, and TNF-alpha.

Front 1256

Risk factors for rupture include Size, COPD, HTN, Rapidly enlarging size, Infection (mycotic aneurysm), Smoking, Female gender.

Front 1257

Annual rupture rates

Back 1257

3-5.5cm 0.6%; 5.6-5.9cm 5-10%

Front 1258

Bloody BM post AAA repair need to R/O ischemic colon (colonoscopy).

Front 1259

Endovascular repair most appropriate in older, higher risk patients b/c long term durability of repair still unproven. Contra-indications to endo AAA repair are short infra-renal neck (<15mm); severe angulation >45 degrees of proximal neck; inadequate iliac landing zone

Front 1260

Serial CT scans for life required post endovascular repair are required to evaluate endoleak

Front 1261

Types of endoleak

Back 1261

I - perigraft flow into the aneurysm sac around the proximal or distial attachment sites; II - collateral blood flow into the aneurysm sac via "back bleeding" patent lumbars or IMA; III - leakage of blood through detached or inadequately sealed segments of a modular graft or through structural defects in the graft material; IV diffusion of blood through microscopic holes in graft material.

Front 1262

Aorto-enteric fistula post AAA repair

Back 1262

tx with extra-anatomic bypass; aortic graft excision with two layered oversew; repair/resect bowel as needed

Front 1264

Thoraco-abdominal Aortic Aeurysms

Front 1265

Crawford Classification of TAAA

Back 1265

I - Aneurysm initiates distal to left sublcavian and terminates proximal to renal vessels; II - initiates just distal to left subclavian and terminates at aortic bifurcation; III - intiates >7cm distal to left subclavian and terminates at aortic bifurcation; IV - initiates below the diaphragm and extends to aortic bifurcation.

Front 1266

Treatment

Back 1266

Repair techniques involve bypass procedure intra-operatively to perfuse distal viscera while working more proximally with short segment of aorta clamped off at a given time for intercostal and visceral vessel reimplantation (bypass augmented clamp and run technique). Repair if thoracic segment greater than 7.5 cm or abdomial component greater than 5.5 cm, or if sympomatic, rapidly enlarging.

Front 1268

Aortic Dissection

Front 1269

Ascending - surgical management due to risk of aortic root rupture.

Front 1270

Descending - medical management with aggressive BP control via B-blk, Hydralazine.

Front 1271

Indications for repair of descending aortic dissection are

Back 1271

compromise of visceral blood flow, rapidly enlarging aneurysmal dilation (size criteria similar to true aneurysms), intractable pain associated with dissection (increased rupture risk).

Front 1273

Dialysis Access

Front 1274

AV fistula with native vessels is the optimal initial permanent access; longer patency relative to AV grafts w/ synthetic material in forearm. Order of access should be 1. radial-cephalic; 2. brachial-cephalic; 3. Basilic vein transposition; 4. Synthetic AV graft

Front 1276

IVC Filter

Front 1277

Indications

Back 1277

PE despite theraputic anticoagulation, DVT or PE with contraindication to full anticoagulation, Persistent DVT (several months) despite full anticoagulation, Following pulmonary embolectomy

Front 1279

Subclavian Steal Syndrome

Front 1280

Etiology

Back 1280

Due to subclavian stenosis proximal to the vertebral artery . When strenously using the arm, vasodilation in the extremity causes reversal of flow in vertebral artery to meet blood supply demand in the arm and can induce vertebrobasilar sx (lightheaded, dizzy, discoordination, pre-syncope)

Front 1281

Treatment

Back 1281

Either angioplasty with or without stenting, or carotid to subclavian bypass

Front 1283

Vasoactive Drugs

Front 1284

Thromboxane A2

Back 1284

potent vasoconstrictor + initiator of platelet aggregation

Front 1285

Prostacyclin

Back 1285

potent inhibitor of platelet aggregation. TXA2 is released by activated platelets.

Front 1286

Aspirin

Back 1286

inhibits TXA2 formation. Therefore is an antiplatelet. Irreversible mechanism of action.

Front 1287

Plavix inhibits platelet aggregation via ADP inhibition.

Front 1288

Nitric Oxide

Back 1288

(endothelial cell-derived relaxation factor) is produced from Larginine and released by endothelium, macrophages, neutrophils, and vascular smooth muscle cells. increases cGMP levels. vasodilator that inhibits platelet aggregation and proliferation of smooth muscle cells and supresses generation of free radicals.

Front 1289

Coumadin

Back 1289

inhibits VitK dependent clotting factors (2, 7, 9 & 10). half life

Front 1290

Heparin

Back 1290

binds and activates antithrombin III. follow PTT levels. half life

Front 1291

Low molecular weight heparin (lovenox)

Back 1291

PTT not followed because of predictable efficacy secondary to decreased binding to serum proteins. Mechanism of action is factor Xa inhibition

Front 1293

Peripheral Vascular Disease

Front 1294

Plaque formation process

Back 1294

1. local accumulation of lipid in vessel wall ( foam cells

Front 1295

Fibromuscular dysplasia

Back 1295

multiple areas of eccentric arterial stenosis alternating with segments of dilitation. Over 90% in females. 80% of renal cases involve right renal artery.

Front 1296

New onset claudication treatment

Back 1296

exercise, smoking cessation, Pletal (Cilostazol) peripherally vasodilates and has antiplatelet effects. Angiography and bypass only after conservative treatment failure

Front 1297

ABI (ankle to brachial index)

Front 1299

Ratio of sytolic blood pressure at pedal vessels (DP/PT) to brachial artery pressure

Front 1300

Normal 1.0-1.2; Claudication associated with 0.5-0.9; Rest pain 0.4 and less

Front 1301

Exercise in pt with PVD results in drop in ABI

Front 1303

Indications for tibial level bypass

Back 1303

Limb Salvage (rest pain and tissue loss). Claudication is not an indication for infrapopliteal bypass.

Front 1304

Best outcome after angioplasty

Back 1304

Common iliac artery

Front 1305

Most common complication of popliteal artery

Back 1305

Emboli. Resect at 2cm.

Front 1307

Arteritis

Front 1308

Takayasu"s Arteritis

Back 1308

most commonly seen in young asian women. Upper extremity occlusive symptoms most common. Aortic arch occlusive dz. Tx with steriods, rarely will operation be required. Giant cell/temporal arteritis also tx with steriods when causing sx before any operation.

Front 1309

Buerger Disease

Back 1309

Inflammatory vasculopathy of medium/small arteries in young male smokers

Front 1310

Diagnosis

Back 1310

Angiography. Will have appearance of “corkscrew collaterals” below the knee.

Front 1311

Treatment

Back 1311

Smoking cessation

Front 1313

Posterior dislocation of the knee

Back 1313

need to get angiogram to rule out popliteal artery disruption (up to 40%).